Note & Notes for MRCP part 1 & 2

1782 Pages·2018·40.69 MB·English

by  Dr. Yousif Abdallah Hamad

Notes & Notes

For MRCP part I & 11

By

Dr. Yousif Abdallah Hamad

1

gmail.com
@
dryousif23

https://www.facebook.com/dryousif23

2

)
The Devil is in the Details
Always Remember (

3

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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By Dr. Yousif Abdallah Hamad
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CNS anatomy

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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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 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
By Dr. Yousif Abdallah Hamad
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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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Notes & Notes for MRCP
By Dr. Yousif Abdallah Hamad
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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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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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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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