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UKMLA Prep > Neurosciences > Flashcards

Neurosciences Flashcards

Conditions and presentation

1
Q

Chorea

A
  • descibes involuntary, rapid, jerky movements from one part of the body to another.
  • caused by damage to the basal ganglia, especially the caudate nuclues.
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2
Q

What are the causes of Chorea

A

Huntington’s disease, Wilson’s disease, ataxic telangiectasia

Sydenham’s chorea
SLE
anti-phospholipid syndrome
rheumatic fever

drugs
oral contraceptive pill, L-dopa, antipsychotics
neuroacanthocytosi

pregnancy: chorea gravidarum
thyrotoxicosis
polycythaemia rubra vera
carbon monoxide poisoning
cerebrovascular disease

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3
Q

Hemiballism

A

Hemiballism occurs following damage to the subthalamic nucleus.

Ballisic movements are involuntary, sudden, jerking movements which occur contralateral to the side of the lesion.

The ballisic movements primarily affect the proximal limb musculature whilst the distal muscles may display more choreiform-like movements

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4
Q

When do Hemiballism symptoms reduce?

A

Patients may have reduced symptoms when they are asleep.

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5
Q

Treatment of Haemiballism?

A

Antidopaminergic agents (e.g. Haloperidol)

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6
Q

Huntington’s disease

A

inherited neurodegenerative condition. It is a progressive and incurable condition that typically results in death 20 years after the initial symptoms develop.

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7
Q

Genetics of Huntington’s disease

A

autosomal dominant
* trinucleotide repeat disorder: repeat expansion of CAG
as Huntington’s disease is a trinucleotide repeat disorder, the phenomenon of anticipation may be seen, where the disease is presents at an earlier age in successive generations
results in degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia
due to defect in huntingtin gene on chromosome 4

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8
Q

Features of Huntingtons which develop after 35

A

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

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9
Q

Oculogyric crisis

A

An oculogyric crisis is a dystonic reaction to certain drugs or medical conditions

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10
Q

Features of Oculogyric crisis

A

restlessness, agitation
involuntary upward deviation of the eyes

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11
Q

causes of oculogyric crisis

A

antipsychotics
metoclopramide
postencephalitic Parkinson’s disease

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12
Q

Managment of oculogyric crisis?

A

cessation of causative medication if possible
intravenous antimuscarinic: benztropine or procyclidine

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13
Q

Restless leg syndrome?

A

syndrome of spontaneous, continuous lower limb movements that may be associated with paraesthesia.

It is extremely common, affecting between 2-10% of the general population. Males and females are equally affected and a family history may be present

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14
Q

Clinical features of restless leg syndrome

A

uncontrollable urge to move legs (akathisia). Symptoms initially occur at night but as condition progresses may occur during the day. Symptoms are worse at rest
paraesthesias e.g. ‘crawling’ or ‘throbbing’ sensations
movements during sleep may be noted by the partner - periodic limb movements of sleeps (PLMS)

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15
Q

causes and associations of restless leg syndrome

A

there is a positive family history in 50% of patients with idiopathic RLS
iron deficiency anaemia
uraemia
diabetes mellitus
pregnancy

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16
Q

blood tests and restless leg syndrome

A

Ferritin to rule out anaemia

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17
Q

Managment of restless leg syndrome

A

simple measures: walking, stretching, massaging affected limbs
treat any iron deficiency
dopamine agonists are first-line treatment (e.g. Pramipexole, ropinirole)
benzodiazepines
gabapentin

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18
Q

Managment of Tics?

A

clonidine
atypical antipsychotics

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19
Q

Wilson’s disease

A

-Autosomal recessive disorder characterised by excessive copper deposition in the tissues.

-Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion.

caused by a defect in the ATP7B gene located on chromosome 13.

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20
Q

incidence of Wilson’s disease?

A

10-25 years
- children will present with liver symptoms first

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21
Q

Signs of Wilson’s disease

A

renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails
Kayser-Fleischer ring
liver hepatitis and cirrhosis

neurological:
basal ganglia degeneration: in the brain, most copper is deposited in the basal ganglia, particularly in the putamen and globus pallidus
speech, behavioural and psychiatric problems are often the first manifestations
also: asterixis, chorea, dementia, parkinsonism

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22
Q

Investigations for Wilson’s disease

A

slit lamp examination for Kayser-Fleischer rings
reduced serum caeruloplasmin
reduced total serum copper
increased 24hr urinary copper excretion
the diagnosis is confirmed by genetic analysis of the ATP7B gene

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23
Q

Managment of Wilson’s disease

A

penicillamine
2nd line is trientine hydrochloride

tetrathiomolybdate is a newer agent that is currently under investigation

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24
Q

when should you refer a child for developmental delay?

A

doesn’t smile at 10 weeks
cannot sit unsupported at 12 months
cannot walk at 18 months
has a hand preference before the age of 12 month

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25
Q

DVLA and CABG

A

4 weeks off driving

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26
Q

DVLA and elective angioplasty

A

1 week off driving

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26
Q

DVLA and hypertension

A

can drive unless treatment causes unacceptable side effects, no need to notify DVLA
if Group 2 Entitlement the disqualifies from driving if resting BP consistently 180 mmHg systolic or more and/or 100 mm Hg diastolic or more

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27
Q

DVLA and ACS

A

4 weeks off driving
1 week if successfully treated by angioplasty

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28
Q

DVLA and angina

A

driving must cease if symptoms occur at rest/at the wheel

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29
Q

DVLA and pacemaker insertion

A

1 week off driving

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30
Q

DVLA and ICD

A

if implanted for sustained ventricular arrhythmia: cease driving for 6 months
if implanted prophylactically then cease driving for 1 month. Having an ICD results in a permanent bar for Group 2 drivers

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31
Q

DVLA and successful catheter abalation for arrhythmia

A

2 days off driving

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32
Q

aortic aneurysm of 6cm or more and DVLA

A

notify DVLA. Licensing will be permitted subject to annual review.

an aortic diameter of 6.5 cm or more disqualifies patients from driving

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33
Q

Heart transplant and DVLA

A
  • 6 weeks dont drive
  • Dont need to tell DVLA
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34
Q

DVLA and HGV

A

Patients who have insulin or other hypoglyacemic drugs must meet following criteria to have HGV

-not been any severe hypoglycaemic event in the previous 12 months

the driver has full hypoglycaemic awareness
the driver must show adequate control of the condition by regular blood glucose monitoring,

at least twice daily and at times relevant to driving
the driver must demonstrate an understanding of the risks of hypoglycaemia
here are no other debarring complications of diabetes

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35
Q

VDIAB1I form

A

patients on insulin who want to apply for a Group 2 (HGV) licence

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36
Q

group 1 drivers diabetes

A

if on insulin then patient can drive a car as long as they have hypoglycaemic awareness, not more than one episode of hypoglycaemia requiring the assistance of another person within the preceding 12 months and no relevant visual impairment. Drivers are normally contacted by DVLA
if on tablets or exenatide no need to notify DVLA. If tablets may induce hypoglycaemia (e.g. sulfonylureas) then there must not have been more than one episode of hypoglycaemia requiring the assistance of another person within the preceding 12 months
if diet controlled alone then no requirement to inform DVLA

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37
Q

Alcohol missuse and DVLA

A

requires licence revocation or refusal until a minimum 6 month period of controlled drinking or abstinence has been attained

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38
Q

Alcohol dependency and DVLA

A

1 year

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39
Q

Cannabis, amphetamines, ecstasy, LSD and DVLA

A

6 month period free of such use has been attained.

Independent medical assessment and urine screen arranged by DVLA, may be required

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40
Q

Heroin, cocaine, methadone and DVLA

A

1 year no driving
need consultant report when reapplying

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41
Q

DVLA and Epilepsy/seizures

A

MUST report to the DVLA

first unprovoked/isolated seizure: 6 months off if there are no relevant structural abnormalities on brain imaging and no definite epileptiform activity on EEG. If these conditions are not met then this is increased to 12 months

for patients with established epilepsy or those with multiple unprovoked seizures:
may qualify for a driving licence if they have been free from any seizure for 12 months
if there have been no seizures for 5 years (with medication if necessary) a ‘til 70 licence is usually restored
withdrawawl of epilepsy medication: should not drive whilst anti-epilepsy medication is being withdrawn and for 6 months after the last dose

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42
Q

Syncope and DVLA

A

simple faint: no restriction
single episode, explained and treated: 4 weeks off
single episode, unexplained: 6 months off
two or more episodes: 12 months off

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43
Q

Stoke/ TIA and DVLA

A

1 month off driving

multiple TIAs over short period of times: 3 months off driving and inform DVLA

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44
Q

craniotomy e.g. For meningioma and DVLA

A

1 year off driving

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45
Q

pituitary tumour: craniotomy and DVLA

A

6 months; trans-sphenoidal surgery ‘can drive when there is no debarring residual impairment likely to affect safe driving’

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46
Q

narcolepsy/cataplexy and DVLA

A

cease driving on diagnosis, can restart once ‘satisfactory control of symptoms

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47
Q

chronic neurological disorders e.g. multiple sclerosis, motor neuron disease and the DVLA

A

DVLA should be informed, complete PK1 form (application for driving licence holders state of health)

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48
Q

psychiatric conditions which must stop driving and inform DVLA

A

agitation, behavioural disturbance or suicidal thoughts
Acute psychotic disorder
Hypomania or mania
Severe disability

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49
Q

conditions where people may drive but need to inform the DVLA (5)

A

Pervasive developmental disorders and ADHD
Mild cognitive impairment
Dementia
Mild learning disability
Personality disorder

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50
Q

Monocular vision and DVLA

A

must notify DVLA
may drive if acuity and visual field is normal in the remaining eye

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51
Q

Blepharospasm and DVLA

A

consultant opinion is required

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52
Q

visual field defects and DVLA

A
  • Cease driving till requirmenrs are met
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53
Q

Differential diagnosis for facial pain

A
  • Trigeminal neuralgia
    -sinusitis
  • dental problems
    -tension-type headaches
  • migraine
    -GCA
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54
Q

Trigeminal neuralgia

A

pain syndrome characterised by severe unilateral pain. The vast majority of cases are idiopathic but compression of the trigeminal roots by tumours or vascular problems may occur.

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55
Q

e International Headache Society definition of trigeminal neuralgia

A
  • unilateral disorder characterised by brief electric shock-like pains, abrupt in onset and termination, limited to one or more divisions of the trigeminal nerve

the pain is commonly evoked by light touch, including washing, shaving, smoking, talking, and brushing the teeth (trigger factors), and frequently occurs spontaneously
small areas in the nasolabial fold or chin may be particularly susceptible to the precipitation of pain (trigger areas)

the pains usually remit for variable periods

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56
Q

Red flag symptoms of TN

A

Sensory changes
Deafness or other ear problems
History of skin or oral lesions that could spread perineurally
Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
Optic neuritis
A family history of multiple sclerosis
Age of onset before 40 years

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57
Q

Managment of TN

A

carbamazepine is first-line
failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology

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58
Q

Down’s syndrome, which neruodegen condition most associated?

A

Alzheimer’s dementia

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59
Q

Seizure

A

spontaneous uncontrolled abnormal brain activity

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60
Q

Epilepsy

A

a tendency to have seizures. Epilepsy is a symptom, and not a true condition. Epilepsy can be diagnosed after a minimum of 2 seizures.

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61
Q

Ictus

A

Can refer to any acute event, in this situation, refers to epilepsy attack itself

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62
Q

Prodome

A

a set of not specific symptoms that precede the onset of a disease, in this case, epilepsy

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63
Q

Prodome

A

a set of not specific symptoms that precede the onset of a disease, in this case, epilepsy

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64
Q

Aura.

A

sensory disturbances that precede an attack, usually just by a few minutes. Can be visual, tactile, olfactory – pretty much any sensation.

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65
Q

Triggers for seizures

A

Sleep deprivation
Alcohol (alcohol intake AND alcohol withdrawal)
Drug misuse
Physical/mental exhaustion
Flickering lights –e.g. on TV/video games – cause primary generalised epilepsy only
Infection / metabolic disturbance
Less common:
Loud noises
Hot bath
Reading
Strange shapes
Strange smells
Strange sounds

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66
Q

Todd’s paralysis

A

Weakness of the links following a seizing

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67
Q

Absent seizures

A

Aka petit mal
childhood onset

Patient unresponsive to stimuli, but still conscious

Patient stares, may go pale
May be some muscle jerking

There is quick recovery after the attack (in petit mal)
They generally last <15s, whereas temporal lobe last >30s.

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68
Q

Tonic clinic seizures

A

Aka grand mal
- often aura before presentation

Tonic phase (10-60s)
Rigidity
Epileptic cry
Tongue biting
Incontinence
Hypoxia/cyanosis – no breathing during this phase
Clonic Phase (seconds-minutes)
Convulsions / limb jerking
Eye rolling
Tachycardia
No breathing / random, uncoordinated breaths

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69
Q

Tonic phase.

A

Lasts 10-60 seconds
Rigidity
Epileptic cry
Tongue biting
Incontinence
Hypoxia/cyanosis – no breathing during this phase

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70
Q

Clonic phase

A

seconds-minutes)
Convulsions / limb jerking
Eye rolling
Tachycardia
No breathing / random, uncoordinated breaths

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71
Q

Status epilepticus

A

Seizure that lasts >30minutes
OR
Multiple seizures, inbetween which, consciousness is not recovered, lasting > 30 minutes

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72
Q

Status epilepticus

A

Seizure that lasts >30minutes
OR
Multiple seizures, inbetween which, consciousness is not recovered, lasting > 30 minutes

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73
Q

What occurs during status epilepticus

A

Electrolyte imbalance as massive energy demands of rapid discharge neurons no longer met
Results in brain swelling and herniation

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74
Q

investigations for seizures

A

ECG
Neurological Exam
Serum Clacium
Urine dipstick – diabetes
EEG
CT/MRI – can show focal lesions
PET scan
Bloods
Sugar – hypoglycaemia
U+E’s – renal problems
Calcium – hypoglycaemia
LFT’s
CK – Serum muscle enzymes – raised in true epileptics after clonus and tonic seizures, normal in pseudoseizures
Serum prolactin – to check for pseudoseizures

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75
Q

Management of seizures

A

Only start after a minimum of two fits. Only use one drug at a time, and begin with a small dose, and gradually increase it, until control is achieved, toxic affects occur, or the maximum dose is reached.

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76
Q

Mechanism of phenobarbital

A

Inhibits sodium channels, thus reducing action potential propagation. Does not lower the seizure threshold.

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77
Q

Side effects of phenobarbital

A

Sedation, impairment of motor and cognition systems after long term use, megaloblastic anaemia

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78
Q

Phenytoin mechanism

A

Inhibits sodium channels, thus reducing action potential propagation. Acts on voltage dependent channels, and selectively binds when they are in the open state.

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79
Q

Side effects Phenytoin

A

Vertigo, nystagmus, headaches, megaloblastic anaemia, hypersensitivity, confusion and cognition problems (high dose). Teratogenic, gum hypertrophy, arrythmias

P- parenthesis (vitamin B12)
H- Hirtsutism
E- encephalopathy
N- nystagmus
Y- yellowing of the skin
T- Tetranogenic
O- osteomalacia
I- gingival hyperplasia
N - neuropathies

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80
Q

When is Phenytoin used

A

Partial and generalised attacks, but not in absence.
High doses my precipitate attacks

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81
Q

What is useful for absent seizures

A

Ethosuximide

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82
Q

What is 2nd line for generalised seizures?

A

Lamotrigine

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83
Q

1st line for partial seizures

A

Carbamazepine

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84
Q

1st line for partial seizures

A

Carbamazepine

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85
Q

When is sodium Valporate used as a first line treatment

A

Absence seizures
– Generalised seizures

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86
Q

Can Sodium Valporate be used in pregnancy?

A

No
Highly teratogenic

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87
Q

What is Wernicke’s aphasia?

A

A type of receptive aphasia due to a lesion of the superior temporal gyrus, characterized by fluent speech, impaired comprehension, and nonsensical sentences.

Typically supplied by the inferior division of the left MCA.

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88
Q

What are the main characteristics of Broca’s aphasia?

A

Non-fluent, labored speech with normal comprehension; caused by a lesion of the inferior frontal gyrus.

Typically supplied by the superior division of the left MCA.

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89
Q

Define conduction aphasia.

A

A type of aphasia resulting from a stroke affecting the arcuate fasciculus, characterized by fluent speech but poor repetition, with normal comprehension.

Patients are aware of their errors.

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90
Q

What is global aphasia?

A

Severe expressive and receptive aphasia due to a large lesion affecting all language areas.

May still communicate using gestures.

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91
Q

What is cerebral palsy?

A

A disorder of movement and posture due to a non-progressive lesion of the motor pathways in the developing brain, affecting 2 in 1,000 live births.

It is the most common cause of major motor impairment.

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92
Q

List the main causes of cerebral palsy.

A
  • Antenatal (80%): cerebral malformation, congenital infection
  • Intrapartum (10%): birth asphyxia/trauma
  • Postnatal (10%): intraventricular hemorrhage, meningitis, head trauma
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93
Q

What are common manifestations of cerebral palsy?

A
  • Abnormal tone in early infancy
  • Delayed motor milestones
  • Abnormal gait
  • Feeding difficulties
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94
Q

What percentage of children with cerebral palsy experience learning difficulties?

A

60%

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95
Q

What is the classification of cerebral palsy based on muscle tone?

A
  • Spastic (70%)
  • Dyskinetic
  • Ataxic
  • Mixed
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96
Q

What is the first-line treatment for essential tremor?

A

Propranolol

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97
Q

What defines febrile convulsions?

A

Seizures provoked by fever in otherwise normal children, typically occurring between 6 months and 5 years.

Seen in 3% of children.

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98
Q

What are the clinical features of febrile convulsions?

A
  • Occur early in a viral infection
  • Usually brief, lasting less than 5 minutes
  • Most commonly tonic-clonic
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99
Q

What is Wernicke’s encephalopathy?

A

A neuropsychiatric disorder caused by thiamine deficiency, often seen in alcoholics, characterized by a classic triad of ophthalmoplegia, ataxia, and encephalopathy.

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100
Q

What are the common features of Wernicke’s encephalopathy?

A
  • Oculomotor dysfunction
  • Nystagmus
  • Gait ataxia
  • Encephalopathy
  • Peripheral sensory neuropathy
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101
Q

What is a transient ischaemic attack (TIA)?

A

A brief period of neurological deficit due to a vascular cause, typically lasting less than an hour.

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102
Q

What are common clinical features of a TIA?

A
  • Unilateral weakness or sensory loss
  • Aphasia or dysarthria
  • Ataxia, vertigo, or loss of balance
  • Visual problems
  • Amaurosis fugax
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103
Q

What is the immediate management for suspected TIA?

A

Give aspirin 300 mg immediately unless contraindicated and assess urgently within 24 hours by a stroke specialist clinician.

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104
Q

What is the primary goal of lipid modification therapy in TIA management?

A

To reduce non-HDL cholesterol by more than 40%.

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105
Q

What are the features of a prolapsed lumbar disc?

A
  • Clear dermatomal leg pain
  • Associated neurological deficits
  • Pain often worse when sitting
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106
Q

What is the classical triad of features in Parkinson’s disease?

A
  • Bradykinesia
  • Tremor
  • Rigidity
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107
Q

What is the epidemiology of Parkinson’s disease?

A

Around twice as common in men.

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108
Q

What is Parkinson’s disease?

A

A progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra.

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109
Q

What are the classical triad of features in Parkinson’s disease?

A
  • Bradykinesia
  • Tremor
  • Rigidity
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110
Q

What is the mean age of diagnosis for Parkinson’s disease?

A

65 years

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111
Q

How does bradykinesia manifest in Parkinson’s disease?

A
  • Poverty of movement (hypokinesia)
  • Short, shuffling steps
  • Reduced arm swinging
  • Difficulty in initiating movement
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112
Q

What characterizes the tremor seen in Parkinson’s disease?

A
  • Most marked at rest
  • 3-5 Hz
  • ‘Pill-rolling’ in thumb and index finger
  • Worse when stressed or tired, improves with voluntary movement
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113
Q

What types of rigidity are observed in Parkinson’s disease?

A
  • Lead pipe rigidity
  • Cogwheel rigidity (due to superimposed tremor)
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114
Q

What are some psychiatric features associated with Parkinson’s disease?

A
  • Depression (most common, affects about 40%)
  • Dementia
  • Psychosis
  • Sleep disturbances
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115
Q

True or False: Drug-induced parkinsonism typically has a slower onset compared to Parkinson’s disease.

A

False

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116
Q

What diagnostic tool does NICE recommend if differentiating between essential tremor and Parkinson’s disease?

A

123I-FP-CIT single photon emission computed tomography (SPECT)

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117
Q

What is the first-line treatment for Parkinson’s disease if motor symptoms affect quality of life?

A

Levodopa

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118
Q

What should be considered if motor symptoms of Parkinson’s disease do not affect quality of life?

A

Dopamine agonist (non-ergot derived), levodopa, or monoamine oxidase B (MAO-B) inhibitor

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119
Q

What are the common adverse events associated with levodopa?

A
  • Dry mouth
  • Anorexia
  • Palpitations
  • Postural hypotension
  • Psychosis
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120
Q

Fill in the blank: The phenomenon where motor activity declines towards the end of the dosage interval is called the _______.

A

end-of-dose wearing off

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121
Q

What are the risks associated with acute akinesia in Parkinson’s medication management?

A

Risk of neuroleptic malignant syndrome

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122
Q

What are the side effects of dopamine receptor agonists?

A
  • Impulse control disorders
  • Excessive daytime somnolence
  • Hallucinations (more likely than levodopa in older patients)
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123
Q

What is myasthenia gravis?

A

An autoimmune disorder resulting in insufficient functioning acetylcholine receptors.

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124
Q

What is the hallmark feature of myasthenia gravis?

A

Muscle fatigability

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125
Q

What is the first-line treatment for myasthenia gravis?

A

Pyridostigmine (long-acting acetylcholinesterase inhibitor)

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126
Q

What are common associations with myasthenia gravis?

A
  • Thymomas (15%)
  • Autoimmune disorders: pernicious anemia, autoimmune thyroid disorders, rheumatoid arthritis, SLE
  • Thymic hyperplasia (50-70%)
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127
Q

What investigations are useful for diagnosing myasthenia gravis?

A
  • Single fibre electromyography
  • CT thorax
  • Antibodies to acetylcholine receptors
  • Tensilon test (not commonly used)
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128
Q

Which drugs may exacerbate myasthenia gravis?

A
  • Penicillamine
  • Quinidine, procainamide
  • Beta-blockers
  • Lithium
  • Phenytoin
  • Antibiotics: gentamicin, macrolides, quinolones, tetracyclines
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129
Q

What is bipolar disorder?

A

A chronic mental health disorder characterised by periods of mania/hypomania alongside episodes of depression.

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130
Q

What is the lifetime prevalence of bipolar disorder?

A

2%.

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131
Q

What are the two types of bipolar disorder?

A
  • Type I disorder: mania and depression
  • Type II disorder: hypomania and depression
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132
Q

Define mania and hypomania.

A

Both terms relate to abnormally elevated mood or irritability; mania includes severe functional impairment or psychotic symptoms for 7 days or more, while hypomania describes decreased or increased function for 4 days or more.

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133
Q

What differentiates mania from hypomania?

A

The presence of psychotic symptoms such as delusions of grandeur or auditory hallucinations suggests mania.

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134
Q

What is the mood stabilizer of choice for managing bipolar disorder?

A

Lithium.

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135
Q

What alternative medication can be used as a mood stabilizer?

A

Valproate.

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136
Q

What is the recommended management for mania/hypomania?

A

Consider stopping antidepressants; antipsychotic therapy such as olanzapine or haloperidol.

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137
Q

What is the recommended management for depression in bipolar disorder?

A
  • Talking therapies
  • Fluoxetine is the antidepressant of choice
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138
Q

What comorbidities are associated with bipolar disorder?

A

Increased risk of diabetes, cardiovascular disease, and COPD.

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139
Q

When should a primary care referral be made for bipolar disorder?

A

If symptoms suggest hypomania, routine referral to CMHT is recommended; urgent referral if there are features of mania or severe depression.

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140
Q

What is the central feature of Chronic Fatigue Syndrome (CFS)?

A

Disabling fatigue affecting mental and physical function more than 50% of the time.

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141
Q

What are common features of CFS?

A
  • Sleep problems
  • Muscle and/or joint pains
  • Headaches
  • Cognitive dysfunction
  • General malaise
  • Dizziness
  • Nausea
  • Palpitations
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142
Q

What investigations are recommended for CFS?

A

A large number of screening blood tests such as FBC, U&E, LFT, glucose, TFT, ESR, CRP, calcium, CK, ferritin, coeliac screening, and urinalysis.

143
Q

What is the management strategy for patients with CFS?

A
  • Refer to a specialist CFS service
  • Energy management strategy
  • Physical activity and exercise under specialist guidance
  • Cognitive behavioural therapy
144
Q

What is fibromyalgia?

A

A syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites.

145
Q

What is the typical demographic affected by fibromyalgia?

A

Women are around 5 times more likely to be affected, typically presenting between 30-50 years old.

146
Q

What are common features of fibromyalgia?

A
  • Chronic pain
  • Lethargy
  • Cognitive impairment (‘fibro fog’)
  • Sleep disturbance
  • Headaches
  • Dizziness
147
Q

How is fibromyalgia diagnosed?

A

Clinically, sometimes using the American College of Rheumatology classification criteria for tender points.

148
Q

What management strategies are suggested for fibromyalgia?

A
  • Aerobic exercise
  • Cognitive behavioural therapy
  • Medications such as pregabalin, duloxetine, amitriptyline
149
Q

What are the early features of Lyme disease?

A
  • Erythema migrans
  • Headache
  • Lethargy
  • Fever
  • Arthralgia
150
Q

What is the first-line test for diagnosing Lyme disease?

A

Enzyme-linked immunosorbent assay (ELISA) for antibodies to Borrelia burgdorferi.

151
Q

What antiviral treatment is recommended for influenza?

A
  • Oseltamivir (first line)
  • Zanamivir (second line)
152
Q

What are the DSM-5 criteria for Major Depressive Disorder (MDD)?

A

Five (or more) symptoms present during the same 2-week period, with at least one being either depressed mood or loss of interest/pleasure.

153
Q

What symptoms are included in the DSM-5 criteria for MDD?

A
  • Depressed mood
  • Diminished interest or pleasure
  • Significant weight change
  • Insomnia or hypersomnia
  • Psychomotor agitation or retardation
  • Fatigue
  • Feelings of worthlessness or guilt
  • Diminished ability to think or concentrate
  • Recurrent thoughts of death or suicide
154
Q

What are the two categories of depression defined by updated NICE guidelines?

A
  • Less severe depression (subthreshold and mild)
  • More severe depression (moderate and severe)
155
Q

What scoring indicates less severe depression on the PHQ-9?

A

A score < 16.

156
Q

What scoring indicates more severe depression on the PHQ-9?

A

A score of ≥ 16.

157
Q

What is insomnia as defined in the DSM-5?

A

Difficulty initiating or maintaining sleep, or early-morning awakening that leads to dissatisfaction with sleep quantity or quality.

158
Q

What are common features associated with insomnia?

A
  • Female gender
  • Increased age
  • Lower educational attainment
  • Unemployment
  • Economic inactivity
  • Widowed, divorced, or separated status
159
Q

What is the short-term management of insomnia?

A
  • Identify potential causes
  • Advise good sleep hygiene
  • Consider hypnotics only if daytime impairment is severe
160
Q

What is the recommendation for using hypnotics in managing insomnia?

A

Use the lowest effective dose for the shortest period possible.

161
Q

What are the recommended hypnotics for treating insomnia?

A
  • Short-acting benzodiazepines
  • Non-benzodiazepines (zopiclone, zolpidem, zaleplon)
162
Q

What features are typically associated with acute insomnia?

A

Typically related to a life event and resolves without treatment.

163
Q

What features are typically associated with chronic insomnia?

A

Trouble falling asleep or staying asleep at least three nights per week for 3 months or longer.

164
Q

What is heart block?

A
165
Q

What is a common neurological condition that can present with facial nerve palsy?

A

Guillain-Barre syndrome

166
Q

What is radicular pain?

A

Pain due to irritation or compression of the spinal root
Follows a dermayome pattern
Feels sharp or shooting

167
Q

What does NICE recommend for diagnosing Lyme disease if erythema migrans is present?

A

Can be diagnosed clinically

168
Q

What is the first-line test for Lyme disease?

A

enzyme-linked immunosorbent assay (ELISA) antibodies to Borrelia burgdorferi

169
Q

If the first ELISA for Lyme disease is negative and symptoms started within 4 weeks, what should be done next?

A

Repeat the ELISA 4-6 weeks after the first test

170
Q

What should be done if Lyme disease is suspected in people with symptoms for 12 weeks or more?

A

An immunoblot test should be done

171
Q

What is the management for asymptomatic tick bites?

A

No routine antibiotic treatment recommended

172
Q

What is the best way to remove a tick?

A

Using fine-tipped tweezers, grasping the tick close to the skin and pulling upwards firmly

173
Q

What antibiotic is recommended for early Lyme disease?

A

Doxycycline

174
Q

What is an alternative antibiotic for Lyme disease if doxycycline is contraindicated?

A

Amoxicillin

175
Q

What should be given for disseminated Lyme disease?

A

Ceftriaxone

176
Q

What reaction may occur after initiating therapy for Lyme disease?

A

Jarisch-Herxheimer reaction

177
Q

What does osteomalacia describe?

A

Softening of the bones secondary to low vitamin D levels

178
Q

What condition is referred to as osteomalacia in growing children?

A

Rickets

179
Q

What are some causes of osteomalacia?

A
  • Vitamin D deficiency
  • Malabsorption
  • Lack of sunlight
  • Diet
  • Chronic kidney disease
  • Drug induced (e.g. anticonvulsants)
  • Inherited (e.g. hypophosphatemic rickets)
  • Liver disease (e.g. cirrhosis)
  • Coeliac disease
180
Q

What are common features of osteomalacia?

A
  • Bone pain
  • Bone/muscle tenderness
  • Fractures (especially femoral neck)
  • Proximal myopathy (may lead to waddling gait)
181
Q

What blood test results are indicative of osteomalacia?

A
  • Low vitamin D levels
  • Low calcium, phosphate (in around 30%)
  • Raised alkaline phosphatase (in 95-100% of patients)
182
Q

What is the initial treatment for osteomalacia?

A

Vitamin D supplementation

183
Q

What is polymyalgia rheumatica (PMR)?

A

A condition characterized by muscle stiffness and raised inflammatory markers

184
Q

What is a typical age range for patients with PMR?

A

Typically > 60 years old

185
Q

What are common symptoms of PMR?

A
  • Aching
  • Morning stiffness in proximal limb muscles
  • Mild polyarthralgia
  • Lethargy
  • Depression
  • Low-grade fever
  • Anorexia
  • Night sweats
186
Q

What are the typical investigation results for PMR?

A

Raised inflammatory markers (e.g. ESR > 40 mm/hr)

187
Q

What is the first-line treatment for PMR?

A

Prednisolone (e.g. 15mg/od)

188
Q

What is the mechanism of action for statins?

A

Inhibit the action of HMG-CoA reductase

189
Q

What are common adverse effects of statins?

A
  • Myopathy (myalgia, myositis, rhabdomyolysis)
  • Liver impairment
  • Increased risk of intracerebral hemorrhage in certain patients
190
Q

What should be monitored when prescribing statins?

A

Liver function tests (LFTs)

191
Q

What are contraindications for statin use?

A
  • Macrolides (e.g. erythromycin)
  • Pregnancy
192
Q

Who should receive a statin?

A
  • All people with established cardiovascular disease
  • Anyone with a 10-year cardiovascular risk >= 10%
  • Patients with type 2 diabetes mellitus
  • Patients with type 1 diabetes diagnosed > 10 years ago or aged over 40
193
Q

When should statins be taken?

A

At night

194
Q

What does systemic lupus erythematosus (SLE) typically present with?

A
  • Fatigue
  • Fever
  • Mouth ulcers
  • Lymphadenopathy
195
Q

What skin manifestations are associated with SLE?

A
  • Malar (butterfly) rash
  • Discoid rash
  • Photosensitivity
  • Raynaud’s phenomenon
  • Livedo reticularis
  • Non-scarring alopecia
196
Q

What are common musculoskeletal symptoms of SLE?

A
  • Arthralgia
  • Non-erosive arthritis
197
Q

What is a common cardiac manifestation of SLE?

A

Pericarditis

198
Q

What is the characteristic feature of Guillain-Barre syndrome?

A

Progressive, symmetrical weakness of all limbs

199
Q

What is the typical initial symptom of Guillain-Barre syndrome?

A

Back/leg pain

200
Q

What is the typical pattern of weakness in Guillain-Barre syndrome?

A

Ascending weakness

201
Q

What is the hallmark investigation finding in Guillain-Barre syndrome?

A

Albuminocytologic dissociation (rise in protein with normal white blood cell count)

202
Q

What are the first-line treatments for diabetic neuropathy?

A
  • Amitriptyline
  • Duloxetine
  • Gabapentin
  • Pregabalin
203
Q

What is gastroparesis?

A

Occurs secondary to autonomic neuropathy

204
Q

What may cause chronic diarrhoea in gastrointestinal autonomic neuropathy?

A

Often occurs at night

205
Q

What is a common drug that can cause peripheral neuropathy?

A

Amiodarone

206
Q

What are the two categories of peripheral neuropathy based on loss type?

A
  • Predominantly motor loss
  • Predominantly sensory loss
207
Q

What is the effect of vitamin B12 deficiency on the spinal cord?

A

Subacute combined degeneration

208
Q

What are the features of dorsal column involvement due to vitamin B12 deficiency?

A
  • Impaired proprioception
  • Vibration sense loss
  • Distal tingling/burning
209
Q

What are the features of Horner’s syndrome?

A
  • Miosis
  • Ptosis
  • Enophthalmos
  • Anhidrosis
210
Q

What is the effect of apraclonidine drops in Horner’s syndrome?

A

Causes pupillary dilation due to denervation supersensitivity

211
Q

What is essential tremor?

A

An autosomal dominant condition affecting both upper limbs

212
Q

What improves essential tremor?

A

Alcohol and rest

213
Q

What is the first-line management for essential tremor?

A

Propranolol

214
Q

What is Alzheimer’s disease?

A

A progressive degenerative disease of the brain accounting for the majority of dementia seen in the UK

Alzheimer’s disease (AD) is primarily characterized by cognitive decline and memory loss.

215
Q

What does NICE recommend for non-pharmacological management of dementia?

A

A range of activities to promote wellbeing tailored to the person’s preference

This includes group cognitive stimulation therapy, reminiscence therapy, and cognitive rehabilitation.

216
Q

What are the three acetylcholinesterase inhibitors recommended for managing mild to moderate Alzheimer’s disease?

A
  • Donepezil
  • Galantamine
  • Rivastigmine

These medications help improve symptoms related to memory and cognition.

217
Q

What is memantine in the context of Alzheimer’s treatment?

A

An NMDA receptor antagonist used as a second-line treatment

It is recommended for patients with moderate Alzheimer’s who cannot tolerate acetylcholinesterase inhibitors.

218
Q

True or False: NICE recommends antidepressants for mild to moderate depression in patients with dementia.

A

False

Antidepressants are not recommended; alternative management strategies should be considered.

219
Q

What are the adverse effects of Donepezil?

A

Insomnia and contraindicated in patients with bradycardia

Monitoring is essential for patients on this medication.

220
Q

What are the risk factors for Alzheimer’s disease?

A
  • Increasing age
  • Family history
  • 5% inherited as autosomal dominant
  • Mutations in amyloid precursor protein
  • Apoprotein E allele E4
  • Caucasian ethnicity
  • Down’s syndrome

Genetic and environmental factors contribute to the risk of developing AD.

221
Q

What are the macroscopic and microscopic pathological changes seen in Alzheimer’s disease?

A

Macroscopic: widespread cerebral atrophy, particularly in the cortex and hippocampus
Microscopic: cortical plaques (A-Beta-amyloid) and neurofibrillary tangles (tau protein)

Hyperphosphorylation of tau protein is linked to AD pathology.

222
Q

What features are indicative of frontotemporal lobar degeneration?

A
  • Onset before 65
  • Insidious onset
  • Preserved memory and visuospatial skills
  • Personality change and social conduct problems

Frontotemporal lobar degeneration includes several types of dementia, notably Pick’s disease.

223
Q

What is Pick’s disease characterized by?

A

Personality change and impaired social conduct

Other symptoms may include hyperorality, disinhibition, and increased appetite.

224
Q

What is the typical onset age for frontotemporal dementia?

A

Before age 65

This type of dementia often presents with personality changes and social conduct problems.

225
Q

What are the common features of Lewy body dementia?

A
  • Progressive cognitive impairment
  • Fluctuating cognition
  • Early impairments in attention and executive function
  • Visual hallucinations

Parkinsonism may also develop in Lewy body dementia patients.

226
Q

What is the diagnostic imaging technique used for Lewy body dementia?

A

Single-photon emission computed tomography (SPECT)

Known commercially as DaTscan, it has a high sensitivity and specificity for diagnosing this condition.

227
Q

What is vascular dementia?

A

A group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage from cerebrovascular disease

It is the second most common form of dementia after Alzheimer’s disease.

228
Q

What are the main subtypes of vascular dementia?

A
  • Stroke-related VD
  • Subcortical VD
  • Mixed dementia

These subtypes are based on underlying causes and clinical presentation.

229
Q

What is the recommended management for vascular dementia?

A

Symptomatic treatment and addressing cardiovascular risk factors

Tailored interventions may include cognitive stimulation and support for patients and caregivers.

230
Q

What characterizes epilepsy?

A

Recurrent seizures

Approximately 500,000 people in the UK are affected by epilepsy.

231
Q

What are the main types of seizures?

A
  • Focal seizures
  • Generalised seizures
  • Unknown onset

Focal seizures may be further classified based on awareness and motor involvement.

232
Q

Fill in the blank: The peak incidence of alcohol withdrawal seizures is at around ______ hours following cessation of drinking.

A

36

Alcohol withdrawal can lead to decreased GABA inhibition and increased glutamate transmission, resulting in seizures.

233
Q

What is the characteristic EEG finding in infantile spasms (West’s syndrome)?

A

Hypsarrhythmia

This syndrome is associated with brief spasms and often has a poor prognosis.

234
Q

What is the typical age range for the onset of Lennox-Gastaut syndrome?

A

1-5 years

This condition may be an extension of infantile spasms and is associated with moderate to severe mental handicap.

235
Q

What is Lennox-Gastaut syndrome?

A

A severe form of epilepsy with onset between 1-5 years, characterized by atypical absences, falls, and jerks, with a poor prognosis and 90% of patients having moderate to severe mental handicap.

EEG shows slow spike activity. Ketogenic diet may help.

236
Q

What are the typical features of benign rolandic epilepsy?

A

Paraesthesia such as unilateral facial sensations, and seizures that characteristically occur at night.

237
Q

What is juvenile myoclonic epilepsy (Janz syndrome)?

A

A type of epilepsy with typical onset in the teens, characterized by infrequent generalized seizures, daytime absences, and sudden shock-like myoclonic seizures, usually responsive to sodium valproate.

238
Q

What symptoms may indicate a generalized seizure?

A

Biting the tongue and experiencing incontinence of urine.

239
Q

What is the postictal phase after a seizure?

A

A phase where patients feel drowsy and tired for around 15 minutes.

240
Q

What investigations are typically performed after a first seizure?

A

An electroencephalogram (EEG) and neuroimaging (usually an MRI).

241
Q

When do most neurologists start prescribing antiepileptics?

A

After a second epileptic seizure.

242
Q

Why is it recommended to prescribe antiepileptics by brand rather than generically?

A

Due to the risk of slightly different bioavailability resulting in a lowered seizure threshold.

243
Q

What is the driving restriction for patients with epilepsy?

A

Patients cannot drive for 6 months following a seizure and must be seizure-free for 12 months before being able to drive.

244
Q

What are some adverse effects of sodium valproate?

A
  • Increased appetite and weight gain
  • Alopecia
  • Ataxia
  • Tremor
  • Hepatitis
  • Pancreatitis
  • Thrombocytopenia
  • Teratogenic effects (neural tube defects)
245
Q

What is the mechanism of action of carbamazepine?

A

Binds to sodium channels increasing their refractory period.

246
Q

What are common adverse effects of lamotrigine?

A

Stevens-Johnson syndrome.

247
Q

What characterizes the acute management of seizures?

A

Most seizures terminate spontaneously, but if they do not terminate after 5-10 minutes, medication is administered, often termed ‘rescue medication’.

248
Q

What is status epilepticus?

A

A medical emergency where seizures continue despite treatment, requiring hospital treatment.

249
Q

How are focal seizures classified?

A
  • Focal aware
  • Focal impaired awareness
  • Awareness unknown
  • Motor
  • Non-motor
250
Q

What are the characteristics of generalized seizures?

A

They engage networks on both sides of the brain at onset, and consciousness is lost immediately.

251
Q

What should women with epilepsy consider regarding pregnancy?

A
  • Effect of contraceptive on anti-epileptic medication
  • Effect of anti-epileptic on contraceptive effectiveness
  • Potential teratogenic effects of anti-epileptics
252
Q

What is the UKMEC classification for women on phenytoin regarding contraception?

A
  • UKMEC 3: COCP and POP
  • UKMEC 2: implant
  • UKMEC 1: Depo-Provera, IUD, IUS
253
Q

What are typical seizure types associated with the temporal lobe?

A

May occur with or without impairment of consciousness, often with an aura and common automatisms.

254
Q

What is the recommended daily dose of folic acid for women considering pregnancy?

A

5mg per day.

255
Q

What are the risks associated with maternal use of sodium valproate during pregnancy?

A

Significant risk of neurodevelopmental delay in children.

256
Q

What is the first-line treatment for generalized tonic-clonic seizures in males?

A

Sodium valproate.

257
Q

What characterizes migraine attacks?

A

Severe, unilateral, throbbing headache associated with nausea, photophobia, and phonophobia, lasting up to 72 hours.

258
Q

What are common triggers for migraine attacks?

A
  • Tiredness
  • Stress
  • Alcohol
  • Lack of food or dehydration
  • Cheese, chocolate, red wine, citrus fruits
  • Menstruation
  • Bright lights
259
Q

What are the diagnostic criteria for migraine without aura?

A
  • At least 5 attacks
  • Headache lasting 4-72 hours
  • At least 2 of: unilateral location, pulsating quality, moderate/severe pain intensity, aggravation by routine physical activity
  • Nausea and/or vomiting or photophobia and phonophobia
  • Not attributed to another disorder
260
Q

What is hemiplegic migraine?

A

A rare variant of migraine where motor weakness is a manifestation of aura.

261
Q

What is the typical duration of auras in migraine patients according to NICE guidelines?

A

5-60 minutes

Auras are fully reversible and develop over at least 5 minutes.

262
Q

What are the common symptoms of migraine aura?

A
  • Transient hemianopic disturbance
  • Spreading scintillating scotoma
  • Sensory symptoms

These symptoms may occur hours prior to the headache.

263
Q

What are some atypical aura symptoms that may prompt further investigation?

A
  • Motor weakness
  • Double vision
  • Visual symptoms affecting only one eye
  • Poor balance
  • Decreased level of consciousness

These symptoms suggest the need for referral or further investigation.

264
Q

What is the first-line treatment for acute migraine attacks?

A
  • Combination therapy with an oral triptan and an NSAID
  • Oral triptan and paracetamol

For young people aged 12-17, consider a nasal triptan in preference to an oral triptan.

265
Q

What should be considered if initial acute migraine treatments are not effective?

A
  • Non-oral preparation of metoclopramide or prochlorperazine
  • Consider adding a non-oral NSAID or triptan

Caution should be exercised when prescribing metoclopramide to young patients due to the risk of acute dystonic reactions.

266
Q

What does NICE recommend for migraine prophylaxis?

A
  • Propranolol
  • Topiramate (avoid in women of childbearing age)
  • Amitriptyline
  • Acupuncture (up to 10 sessions over 5-8 weeks)

Riboflavin (400 mg once a day) may also be effective in reducing migraine frequency and intensity.

267
Q

What is the prognosis for patients with motor neuron disease?

A

Poor: 50% of patients die within 3 years

Motor neuron disease is a progressive condition with various patterns including ALS, progressive muscular atrophy, and bulbar palsy.

268
Q

What are the common presentations of amyotrophic lateral sclerosis (ALS)?

A
  • Asymmetric limb weakness
  • Mixture of lower and upper motor neuron signs
  • Wasting of small hand muscles/tibialis anterior
  • Fasciculations
  • Absence of sensory signs/symptoms

Vague sensory symptoms may occur early but never sensory signs.

269
Q

What is the first-line treatment for migraine during pregnancy?

A

Paracetamol 1g

NSAIDs can be used second-line in the first and second trimester, but aspirin and opioids such as codeine should be avoided.

270
Q

Which conditions are associated with predominantly motor loss in peripheral neuropathy?

A
  • Guillain-Barre syndrome
  • Porphyria
  • Lead poisoning
  • Hereditary sensorimotor neuropathies (Charcot-Marie-Tooth)
  • Chronic inflammatory demyelinating polyneuropathy (CIDP)
  • Diphtheria

These conditions primarily affect motor function rather than sensory function.

271
Q

What are the common causes of predominantly sensory loss in peripheral neuropathy? (6)

A
  • Diabetes
  • Uraemia
  • Leprosy
  • Alcoholism
  • Vitamin B12 deficiency
  • Amyloidosis

These conditions typically lead to sensory loss rather than motor loss.

272
Q

What is the most common form of multiple sclerosis?

A

Relapsing-remitting disease

This form accounts for around 85% of patients and involves acute attacks followed by periods of remission.

273
Q

What is the typical management for chronic diarrhoea due to gastrointestinal autonomic neuropathy?

A

Often occurs at night

Management may require addressing the underlying autonomic neuropathy.

274
Q

What is the role of riluzole in motor neuron disease?

A

Prevents stimulation of glutamate receptors; used mainly in ALS to prolong life by about 3 months

It is not a cure but can help manage the condition.

275
Q

What are the common symptoms of vitamin B12 deficiency?

A
  • Dorsal column involvement
  • Distal tingling/burning/sensory loss
  • Impaired proprioception and vibration sense
  • Muscle weakness
  • Hyperreflexia
  • Spasticity

Symptoms typically develop in the legs before the arms.

276
Q

What are the key features of multiple sclerosis diagnosis?

A
  • Two or more relapses
  • Objective clinical evidence of two or more lesions or one lesion with reasonable historical evidence of a previous relapse

MRI and CSF analysis can support the diagnosis.

277
Q

What is muscular dystrophy primarily caused by?

A

Mutation in the gene encoding dystrophin

The dystrophin gene is located on Xp21.

278
Q

What role does dystrophin play in muscle cells?

A

Connects the muscle membrane to actin, part of the muscle cytoskeleton

279
Q

What type of mutation leads to Duchenne muscular dystrophy?

A

Frameshift mutation

This mutation results in one or both binding sites being lost.

280
Q

What type of mutation leads to Becker muscular dystrophy?

A

Non-frameshift insertion

This mutation preserves both binding sites and leads to a milder form.

281
Q

At what age do features of muscular dystrophy typically develop?

A

After the age of 10 years

282
Q

True or False: Intellectual impairment is much more common in Duchenne muscular dystrophy than in Becker muscular dystrophy.

A

False

283
Q

What is Duchenne muscular dystrophy classified as?

A

An X-linked recessive inherited disorder

284
Q

What are the initial symptoms of Duchenne muscular dystrophy?

A

Progressive proximal muscle weakness from 5 years

Calf pseudohypertrophy is also common.

285
Q

What is Gower’s sign?

A

Child uses arms to stand up from a squatted position

286
Q

What percentage of Duchenne muscular dystrophy patients have intellectual impairment?

A

30%

287
Q

What is a key investigation finding for muscular dystrophy?

A

Raised creatinine kinase

288
Q

What has replaced muscle biopsy for definitive diagnosis of muscular dystrophy?

A

Genetic testing

289
Q

What is the management approach for muscular dystrophy?

A

Largely supportive

There is currently no effective treatment.

290
Q

What is the typical prognosis for children with Duchenne muscular dystrophy regarding mobility?

A

Most cannot walk by the age of 12 years

291
Q

What is the typical life expectancy for patients with Duchenne muscular dystrophy?

A

Around 25-30 years

292
Q

What cardiac condition is associated with Duchenne muscular dystrophy?

A

Dilated cardiomyopathy

293
Q

What is myotonic dystrophy also known as?

A

Dystrophia myotonica

294
Q

At what age do features of myotonic dystrophy typically develop?

A

Around 20-30 years old

295
Q

What type of genetic inheritance does myotonic dystrophy follow?

A

Autosomal dominant

296
Q

What is the cause of DM1?

A

CTG repeat at the end of the DMPK gene on chromosome 19

297
Q

What is the cause of DM2?

A

Repeat expansion of the ZNF9 gene on chromosome 3

298
Q

Fill in the blank: DM1 is caused by a CTG repeat at the end of the _______ gene.

A

DMPK

299
Q

List the key differences between DM1 and DM2.

A
  • DM1: DMPK gene on chromosome 19
  • DM1: Distal weakness more prominent
  • DM2: ZNF9 gene on chromosome 3
  • DM2: Proximal weakness more prominent
  • Severe congenital form not seen in DM2
300
Q

What are common general features of myotonic dystrophy? (5)

A
  • Myotonic facies
  • Frontal balding
  • Bilateral ptosis
  • Cataracts
  • Dysarthria
301
Q

What are other features of myotonic dystrophy? (6)

A
  • Myotonia
  • Weakness of arms and legs
  • Mild mental impairment
  • Diabetes mellitus
  • Testicular atrophy
  • Cardiac involvement
302
Q

What cardiac issues can arise in myotonic dystrophy?

A
  • Heart block
  • Cardiomyopathy
303
Q

What swallowing issue is associated with myotonic dystrophy?

A

Dysphagia

304
Q

What are the main functions of the basal ganglia?

A

Motor control, learning, and emotions

The key nuclei involved include the caudate nucleus, putamen, globus pallidus, subthalamic nucleus, and substantia nigra.

305
Q

Name the components of the basal ganglia. (5)

A
  • Caudate nucleus
  • Putamen
  • Globus pallidus (external and internal segments)
  • Subthalamic nucleus
  • Substantia nigra

The substantia nigra has two parts: pars compacta (produces dopamine) and pars reticulata (regulates motor output).

306
Q

What is the function of the thalamic nuclei?

A

Relay sensory and motor signals, and regulate consciousness and alertness

Important nuclei include the anterior nucleus, ventral anterior/ventral lateral nuclei, and medial geniculate nucleus.

307
Q

What role does the anterior nucleus of the thalamus play?

A

Part of the limbic system, involved in memory

It is one of the thalamic nuclei.

308
Q

Fill in the blank: The _______ nucleus is responsible for visual relay to the occipital cortex.

A

Lateral geniculate nucleus (LGN)

The LGN is crucial for processing visual information.

309
Q

Which hypothalamic nucleus produces ADH?

A

Supraoptic nucleus

ADH is also known as vasopressin.

310
Q

What is the function of the paraventricular nucleus?

A

Produces oxytocin and CRH

CRH stands for corticotropin-releasing hormone.

311
Q

List the main functions controlled by hypothalamic nuclei.

A
  • Autonomic functions
  • Endocrine functions
  • Behavioral functions

Various nuclei regulate different aspects such as hunger, satiety, and circadian rhythms.

312
Q

What is the role of the red nucleus in the midbrain?

A

Motor coordination

It is involved in the control of limb movements.

313
Q

True or False: The periaqueductal gray is involved in pain modulation.

A

True

This region is critical for the descending modulation of pain.

314
Q

What do the pontine nuclei do?

A

Relay signals from the cortex to the cerebellum

This communication is essential for motor coordination.

315
Q

Fill in the blank: The _______ nucleus coordinates motor activity and is located in the medulla.

A

Inferior olivary nucleus

It plays a key role in motor learning and coordination.

316
Q

What is the function of the dentate nucleus in the cerebellum?

A

Coordinates fine movements

It is one of the key cerebellar nuclei involved in motor control.

317
Q

Which limbic system nucleus is critical for emotion and fear processing?

A

Amygdala

The amygdala is essential for emotional responses.

318
Q

What is the primary function of the hippocampus?

A

Memory consolidation

It plays a significant role in forming new memories.

319
Q

What do the dorsal column nuclei relay to the brainstem?

A

Proprioception and vibration

The gracile and cuneate nuclei are part of this system.

320
Q

What is the function of cranial nerve I?

A

Smell

Olfactory nerve

321
Q

What is the pathway for cranial nerve II?

A

Optic canal

This nerve is responsible for sight.

322
Q

Which cranial nerve is responsible for eye movement and pupil constriction?

A

Cranial nerve III (Oculomotor)

Palsy results in ptosis, ‘down and out’ eye, and dilated, fixed pupil.

323
Q

What is the clinical result of a palsy in cranial nerve III?

A

Ptosis, ‘down and out’ eye, dilated and fixed pupil

This indicates dysfunction in eye movement and pupil control.

324
Q

What is the function of cranial nerve IV?

A

Eye movement (Superior Oblique)

Palsy results in defective downward gaze and vertical diplopia.

325
Q

What is the pathway for cranial nerve V?

A

V1: Superior orbital fissure, V2: Foramen rotundum, V3: Foramen ovale

This nerve is responsible for facial sensation and mastication.

326
Q

What are the clinical implications of lesions in cranial nerve V?

A

Trigeminal neuralgia, loss of corneal reflex (afferent), loss of facial sensation, paralysis of mastication muscles, deviation of jaw to weak side

These indicate various dysfunctions related to sensation and movement.

327
Q

What is the function of cranial nerve VI?

A

Eye movement (Lateral Rectus)

Palsy results in defective abduction and horizontal diplopia.

328
Q

What are the functions of cranial nerve VII?

A

Facial movement, taste (anterior 2/3rds of tongue), lacrimation, salivation

Lesions may result in flaccid paralysis of upper and lower face, loss of corneal reflex (efferent), loss of taste, and hyperacusis.

329
Q

What is the clinical result of lesions in cranial nerve VIII?

A

Hearing loss, vertigo, nystagmus

Acoustic neuromas are Schwann cell tumors of the cochlear nerve.

330
Q

What is the function of cranial nerve IX?

A

Taste (posterior 1/3rd of tongue), salivation, swallowing, mediates input from carotid body & sinus

Lesions may cause hypersensitive carotid sinus reflex and loss of gag reflex (afferent).

331
Q

What is the pathway for cranial nerve X?

A

Jugular foramen

This nerve is involved in phonation, swallowing, and innervates viscera.

332
Q

What is the clinical result of lesions in cranial nerve X?

A

Uvula deviates away from site of lesion, loss of gag reflex (efferent)

This indicates dysfunction in swallowing and reflex responses.

333
Q

What is the function of cranial nerve XI?

A

Head and shoulder movement

Lesions may result in weakness turning head to contralateral side.

334
Q

What is the function of cranial nerve XII?

A

Tongue movement

Tongue deviates towards side of lesion.

335
Q

Which cranial nerves are primarily sensory?

A

I (Olfactory), II (Optic), VIII (Vestibulocochlear)

These nerves are primarily responsible for sensory functions.

336
Q

Which cranial nerves are primarily motor?

A

III (Oculomotor), IV (Trochlear), VI (Abducens), XI (Accessory), XII (Hypoglossal)

These nerves are primarily responsible for motor functions.

337
Q

Fill in the blank: Some Say Marry Money But My Brother Says _______.

A

Big Brains Matter Most

This mnemonic helps remember the sensory/motor/both classification of cranial nerves.

338
Q

What is the afferent limb of the corneal reflex?

A

Ophthalmic nerve (V1)

The efferent limb is the Facial nerve (VII).

339
Q

What is the efferent limb of the gag reflex?

A

Vagal nerve (X)

The afferent limb is the Glossopharyngeal nerve (IX).

340
Q

What is the afferent limb of the pupillary light reflex?

A

Optic nerve (II)

The efferent limb is the Oculomotor nerve (III).

341
Q

What ligament connects the tips of spinous processes?

A

Supraspinous ligament

The supraspinous ligament is a strong, fibrous band that runs along the tips of the spinous processes of the vertebrae.

342
Q

What are the ligaments called that are found between adjacent borders of spinous processes?

A

Interspinous ligaments

The interspinous ligaments are situated between the spinous processes of adjacent vertebrae.

343
Q

What ligament is penetrated after the supraspinous and interspinous ligaments during the procedure?

A

Ligamentum flavum

The ligamentum flavum is a thick elastic ligament that connects the laminae of adjacent vertebrae.

344
Q

What indicates the penetration of the needle through the dura mater?

A

A second give

This second give is a tactile sensation felt when the needle passes through the dura mater.

345
Q

What fluid should be obtained after penetrating the dura mater into the subarachnoid space?

A

Clear CSF

Clear cerebrospinal fluid (CSF) is a sign that the needle has entered the subarachnoid space.

347
Q

How are the brachial plexus cords described?

A

According to their relationship with the axillary artery.

348
Q

Where do the brachial plexus cords pass in relation to the rib and lung?

A

Over the 1st rib near to the dome of the lung.

349
Q

What structure do the brachial plexus cords pass beneath?

A

The clavicle immediately posterior to the subclavian artery.

350
Q

What forms the lateral cord of the brachial plexus?

A

Anterior divisions of the upper and middle trunks.

351
Q

What is the origin of the lateral pectoral nerve?

A

C5, C6, C7.

352
Q

What forms the medial cord of the brachial plexus?

A

Anterior division of the lower trunk.

353
Q

List the nerves that originate from the medial cord.

A
  • Medial pectoral nerve (C8, T1)
  • Medial brachial cutaneous nerve (T1)
  • Medial antebrachial cutaneous nerve (C8, T1)
354
Q

What forms the posterior cord of the brachial plexus?

A

Posterior divisions of the 3 trunks (C5-T1).

355
Q

List the nerves that originate from the posterior cord.

A
  • Upper subscapular nerve (C7, C8)
  • Lower subscapular nerve (C5, C6)
  • Thoracodorsal nerve (C6, C7, C8)
  • Axillary nerve
  • Radial nerve
356
Q
A
357
Q

What does the mnemonic BEST stand for in relation to radial nerve muscles?

A
  • Brachioradialis
  • Extensors
  • Supinator
  • Triceps

This mnemonic helps in remembering the key muscles innervated by the radial nerve.

UKMLA Prep (46 decks)

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