Table Of ContentNotes & Notes
For MRCP part I & 11
By
Dr. Yousif Abdallah Hamad
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@
dryousif23
https://www.facebook.com/dryousif23
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)
The Devil is in the Details
Always Remember (
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The main Sources of this Notes & Notes
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Notes & Notes for MRCP By Dr. Yousif Abdallah Hamad
The contents
Section
Page
Neurology
5
Endocrinology
180
Cardiology
464
Respiratory
608
Gastroenterology
794
Renal
925
Rheumatology
1035
Haematology
1134
Infectious
1245
Minor
Dermatology
1354
Ophthalmology
1427
Psychiatry
1479
Basics
Cell biology
1517
Biochemistry and metabolism
1543
Immunology
1581
Genetics
1635
Statistics
1665
Pharmacology
1694
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Neurology
Notes & Notes for MRCP
By Dr. Yousif Abdallah Hamad
1
Notes & Notes
For MRCP part 1 & 11
By
Dr. Yousif Abdallah Hamad
Neurology
Updated
2017
Contains:
1/ Passmedicine 2017
2/ On examination 2017
3/ Pastest 2017
4/ Red fonts --> previous exams
5/ Other updated UK sources
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Neurology
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CNS anatomy
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Notes & Notes for MRCP
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Foramina of the skull
Questions asking about foramina of the skull have come up in the exam in previous years. Below is a
brief summary of the major foramina:
Foramen
Bone
Vessels
Nerves
Optic canal
Sphenoid
Ophthalmic artery
Optic nerve (II)
Superior
orbital
fissure
Sphenoid
Superior ophthalmic vein
Inferior ophthalmic vein
Oculomotor nerve (III)
Trochlear nerve (IV)
lacrimal, frontal and nasociliary
branches of ophthalmic nerve (V: V1)
Abducent nerve (VI)
Inferior
orbital
fissure
Sphenoid
and maxilla
Inferior ophthalmic veins
Infraorbital artery
Infraorbital vein
Zygomatic nerve and infraorbital
nerve of maxillary nerve (V2)
Orbital branches of pterygopalatine
ganglion
Foramen
rotundum
Sphenoid
-
Maxillary nerve (V2)
Foramen
ovale
Sphenoid
Accessory meningeal artery
Mandibular nerve (V3)
Jugular
foramen
Occipital and
temporal
Posterior meningeal artery
Ascending pharyngeal artery
Inferior petrosal sinus
Sigmoid sinus
Internal jugular vein
Glossopharyngeal nerve (IX)
Vagus nerve (X)
Accessory nerve (XI)
Right jugular foramen lesion:
palatal weakness and swallowing difficulties (IX/X),
shoulder and sternocleidomastoid weakness (due to accessory nerve (XI) involvement.
Anatomy
hindbrain comprises:
myelencephalon (medulla oblongata and lower part of the fourth ventricle)
medulla oblongata opens into the fourth ventricle.
metencephalon (pons, cerebellum and intermediate part of fourth ventricle), and
Isthmus rhombencephalon.
Cranial nerve nucleus
All the nuclei except that of the trochlear nerve (CN IV) supply nerves of the same side of
the body.
nucleus ambiguous
gives rise to fibres of the glossopharyngeal (IX), vagus (X), and accessory (XI)
nerves.
Solitary nucleus
embedded in the medulla oblongata,
purely sensory nuclei
receives inputs from cranial nerves: facial (VII), glossopharyngeal (IX) and vagus (X).
involved in the reflexes initiated through the vagus or glossopharyngeal nerves
(e.g., carotid sinus reflex, gag reflex, etc.).
specifically receives:
Taste information from the facial nerve (anterior 2/3 of the tongue),
glossopharyngeal nerve (posterior 1/3) and vagus nerve (small area on the
epiglottis)
general visceral sensory inputs from the chemoreceptors in the carotid body (via
glossopharyngeal nerve) and aortic body (via vagus nerve) and baroreceptors in
the carotid sinus (via glossopharyngeal nerve)
general visceral sensory inputs from mechanoreceptors and chemoreceptors
located in the heart, lungs and gastrointestinal tract (via vagus nerve).
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Neurology
Notes & Notes for MRCP
By Dr. Yousif Abdallah Hamad
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Nucleus locus coeruleus
located in the pons
involved with the physiological responses to stress and panic.
the principal site for brain synthesis of norepinephrine (noradrenaline).
Norepinephrine also released from the adrenal medulla.
Melanin granules inside the neurons contribute to its blue colour.
In opiate withdrawal:
Opioids inhibit the firing of neurons in the locus coeruleus.
opiate withdrawal increased activity of the locus coeruleus withdrawal
symptoms.
clonidine (alpha2 adrenoceptor agonist) is used to counteract this
withdrawal effect by decreasing adrenergic neurotransmission from the
locus coeruleus
Brain lesions
The following neurological disorders/features may allow localisation of a brain lesion:
Frontal lobes lesions
Difficulties with task sequencing and executive skills
Expressive (Broca's) aphasia:
located on the posterior aspect of the frontal lobe, in the inferior frontal gyrus.
Speech is non-fluent, laboured, and halting
Disinhibition
Perseveration
Anosmia
primitive reflexes (positive grasp, pout and palmomental reflexes)
inability to generate a list
Changes in personality.
Parietal lobes lesions
sensory inattention (contralateral hemihypesthesia)
apraxias
astereognosis (tactile agnosia)
inferior homonymous quadrantanopia
Neglect
mild hemiparesis
parietal ataxia
Acalculia (inability to perform mental arithmetic).
Gerstmann's syndrome (lesion of dominant parietal):
Alexia (inability to read), acalculia, finger agnosia and right-left disorientation
unilateral impairment of optokinetic nystagmus.
Optokinetic nystagmus is a nystagmus that occurs in response to a rotation movement.
It is present normally.
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Neurology
Notes & Notes for MRCP
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Temporal lobes lesions
Homonymous quadrantanopias
PITS
(Parietal-Inferior, Temporal-Superior)
Wernicke's aphasia:
this area 'forms' the speech before 'sending it' to Broca’s area.
Lesions result in word substitution, neologisms but speech remains fluent
superior homonymous quadrantanopia
auditory agnosia
prosopagnosia (difficulty recognising faces)
Memory impairment.
Occipital lobes lesions
homonymous hemianopia (with macula sparing)
may present as Anton syndrome where there is blindness but the patient is unaware or
denies blindness.
cortical blindness
visual agnosia
visual illusions and elementary visual hallucinations.
May 2010 exam: A patient diagnosed with a glioma in the parietal lobe. Which feature is
most likely to develop? Acalculia
Cerebellum lesions
midline lesions:
gait and truncal ataxia
hemisphere lesions:
intention tremor,
past pointing,
dysdiadokinesis (inability to perform rapid, alternating movements),
nystagmus
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Neurology
Notes & Notes for MRCP
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More specific areas
Area
Associated conditions
Medial thalamus and
mammillary bodies of the
hypothalamus
Wernicke and Korsakoff’s syndrome
Subthalamic nucleus of the basal
ganglia
Hemiballism
Striatum (caudate nucleus) of the
basal ganglia
Huntington chorea
Substantia nigra of the basal
ganglia
Parkinson's disease
Amygdala
Kluver-Bucy syndrome:
hypersexuality,
hyperorality (insertion of inappropriate objects in the mouth)
hyperphagia,
visual agnosia
increased activation to the amygdala is associated with depression
Hippocampus pathology
Short term memory impairment (for example, Alzheimer's
disease).
Lateral geniculate nucleus
pathology
visual field defect.
Red nucleus
tremor, which is present both at rest and during action (for
example, multiple sclerosis tremor).
Prefrontal cortex damage
disinhibition and problems with social interaction and
judgement and has been implicated in schizophrenia.
Left prefrontal cortex Depression
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Neurology
Notes & Notes for MRCP
By Dr. Yousif Abdallah Hamad
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Transient ischaemic attack (TIA)
Definition
temporary, focal cerebral ischemia that results in brief neurologic deficits lasting < 24 hours
Stroke risk assessment
ABCD2 prognostic score
ABCD2 score is used to determine the risk for stroke in the days following a (TIA)
This gives a total score ranging from 0 to 7.
Criteria
Points
A
Age >= 60 years
1
B
Blood pressure >= 140/90 mmHg
1
C
Clinical features
- Unilateral weakness
- Speech disturbance, no weakness
2
1
D
Duration of symptoms
- > 60 minutes
- 10-59 minutes
2
1
Patient has diabetes
1
Interpretation of ABCD2 risk score
If the ABCD2 risk score is 4 or above high risk of stroke
should have:
aspirin (300 mg daily) started immediately
specialist assessment and investigation within 24 hours of onset of
symptoms
measures for secondary prevention introduced as soon as the
diagnosis is confirmed, including discussion of individual risk factors
If the ABCD2 risk score is 3 or below low risk of stroke
specialist assessment within 1 week of symptom onset, including decision on brain
imaging
if vascular territory or pathology is uncertain, refer for brain imaging
People with crescendo TIAs (two or more episodes in a week) should be treated as being
at high risk of stroke, even though they may have an ABCD2 score of 3 or below.
The risk for stroke can be estimated from the ABCD2 score as follows:
2 day risk
7 day risk
Score 1-3 (low)
1.0%
1.2%
Score 4-5 (moderate)
4.1%
5.9%
Score 6–7 (high)
8.1%
11.7%
The Risk of future ischemic stroke after a TIA
overall annual risk is 3–4%,
over the next 7 days is 11%
over the following 5 years is 24–29%.
Ref: emedicine.medscape.com Updated: Sep 11, 2017
https://emedicine.medscape.com/article/1910519-overview
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By Dr. Yousif Abdallah Hamad
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A 77-year-old man presented after a single episode of unilateral weakness of the left arm that lasted
for 2 hours. 170/100 mmHg. What is his chance of having a stroke in the first week? 11%
Ref: www.mrcpuk.org/ Acute Medicine Specialty Certificate Examination/ sample questions
Investigations (NICE guidelines. Last updated: March 2017 )
Most specific and sensitive for TIA
MRI is superior to CT in detecting the small ischemic lesions occurring after TIA and
minor stroke.
Identifies ischemia earlier than CT (within 3–30 minutes after onset)
Non-contrast cranial CT (gold standard and most important initial imaging in
stroke):
detects acute hemorrhage but cannot reliably identify early
ischemia
CT scanning should only be used if MRI is contraindicated
Although the definition of TIA is "a transient episode of neurological dysfunction caused
by focal brain, spinal cord, or retinal ischemia, without acute infarction," up to 50% of TIA
show ischemic changes in imaging.
MRI findings of ischemia
T1: hypointense
T2: hyperintense
Time of image:
ABCD2 score ≥ 4 urgent brain imaging within 24 hours (preferably diffusion-
weighted MRI)
the most appropriate next step Admit for MRI neuroimaging,
initiate anti-platelet therapy
ABCD2 score ≤ 4 brain imaging (preferably diffusion-weighted MRI) within 1
week
Duplex ultrasound of carotid stenosis
the most appropriate next step if bruits in the neck are heard upon auscultation.
If ultrasound is not available, a CTA or MRA may be used.
Treatment
Antithrombotic therapy (2012 Royal College guideline)
clopidogrel is recommended first-line (as for patients who've had a stroke)
aspirin + dipyridamole should be given to patients who cannot tolerate clopidogrel
2016 Royal College guideline
Patients with a confirmed diagnosis of TIA should receive clopidogrel (300 mg loading dose
and 75 mg daily thereafter) and high intensity statin therapy (e.g. atorvastatin 20-80 mg daily)
started immediately.
January 2013 exam: Which factor is most associated with an increased risk of going on to
have a stroke in a patient presented with TIA? Duration of his TIA
Stroke
Etiology
35% - atherosclerosis of the extracranial vessels (carotid atheroma)
30% - cardiac and fat emboli, endocarditis
15% - lacunar
10% - parenchymal hemorrhage
10% - subarachnoid hemorrhage
Presentation
Edema occurs 2-4 days post-infarct.
Watch for symptoms
decorticate (cortical lesion): flexion of arms
decerebrate (midbrain or lower lesion): extension of arms
cerebellar: ataxia, nystagmus, abnormal finger-nose and heel-shin
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Neurology
Notes & Notes for MRCP
By Dr. Yousif Abdallah Hamad
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Other stroke syndromes
lateral medullary infarct (Wallenburg syndrome)
loss of pain and temp on ipsilateral face and contralateral body, vestibulocerebellar
impairment, Horner's syndrome
Imaging
CT without contrast for acute presentation
the next best step in the management of stroke
to rule out hemorrhage
Contrast head CT is not used in the diagnosis of acute stroke.
if the CT is negative MRI, specifically diffusion-weighted imaging and others, is the most
widely used.
MR studies may show which brain regions are already infarcted and which are at risk of
infarction if perfusion is not restored.
An acute ischemic stroke is diagnosed by diffusion weighted MRI or by using the clinical
history (i.e. don't delay tPA just to get an MRI if there is strong clinical suspicion and no
evidence of bleed).
Management
If an ischemic stroke suspected clinically and CT is negative for evidence of a hemorrhagic
stroke, the recommended treatment is to give IV tPA if the presentation is within 3-4.5 hours.
Of note, a contraindication to tPA is systolic BP > 185 or diastolic BP > 110 mm Hg.
For embolic disease and hypercoagulable states give warfarin or aspirin only once the
hemorrhagic stroke has been ruled out.
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Neurology
Notes & Notes for MRCP
By Dr. Yousif Abdallah Hamad
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__________________________________________________________________
Stroke by anatomy
Site of the lesion
Associated effects
Anterior cerebral artery
Contralateral hemiparesis and sensory loss, lower
extremity > upper
Middle cerebral artery
Contralateral hemiparesis and sensory loss, upper
extremity > lower
Contralateral homonymous hemianopia
Aphasia (global aphasia)
Posterior cerebral artery
Contralateral homonymous hemianopia with macular
sparing
Visual agnosia
Other possible findings:
Cortical blindness
Visual hallucinations
Thalamic syndrome, and
Claude's and Weber's syndromes.
Weber's syndrome (branches of the posterior
cerebral artery that supply the midbrain)
Or branches of the basilar artery
Ipsilateral CN III palsy
Contralateral weakness
Posterior inferior cerebellar artery
(PICA)(lateral medullary syndrome,
Wallenberg syndrome)
lesion to dorsolateral medulla
Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss.
Ataxia, nystagmus
Anterior inferior cerebellar artery (lateral
pontine syndrome)
Symptoms are similar to Wallenberg's (see above), but:
Ipsilateral: facial paralysis and deafness
Retinal/ophthalmic artery
Amaurosis fugax
Basilar artery
'Locked-in' syndrome
__________________________________________________________________
Middle cerebral artery (MCA) occlusion
For individuals aged up to 60 years who suffer an acute MCA territory ischaemic stroke
complicated by massive cerebral oedema, surgical decompression by hemicraniectomy
should be offered within 48 hours of stroke onset.
Divisions
Superior division
Occlusion of the superior division of the MCA results in:
contralateral hemiparesis that affects the face, hand and arm, but spares the
leg
contralateral hemisensory deficit in the same distribution
no homonymous hemianopia
If the dominant hemisphere is involved, there is also expressive aphasia
Inferior division
Occlusion of the inferior division of the middle cerebral artery results in:
contralateral homonymous hemianopia
marked impairment of cortical sensory functions, such as graphaesthesia
and stereognosis on the contralateral side of the body
disorders of spatial thought, including
lack of awareness that a deficit exists (anosognosia)
neglect of and failure to recognise the contralateral limbs
neglect of the contralateral side of external space
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