Paper 2 Flashcards
(36 cards)
Describe what is meant by the multi-site closure of the neural tube in humans (3marks) and explain
the implications with respect to the clinical presentation of neural tube defects (7 marks). You may
use a set of well labelled diagrams as your answer.
Students should give a general description of the closure of the neural tube that is classically covered in
embryology texts for vertebrates. The induction by the notochord of the overlying neuroectoderm / neural
plate to form neural folds and groove, then roll up and form neural tube / neurulation. Fusion occurring
from the middle of the developing trunk of the body in a cranial and caudal direction. The last points of
fusion are the rostral and caudal neuropores. Expand on this by describing the different sites of closure of
the neural tube in the human embryo, covering the sequence as reflected in the diagram on the right and
explaining the meaning of the directions of the arrow heads. They should explain the difference between
primary and secondary neurulation. Finally, explain how the meeting points of the tips of the arrow heads
will indicate the most common points where a NTD may occur.
Describe the change in position of the grey matter (neurones) with respect to the white matter (fibres)
in the developing neural tube at the level of the rhombencephalon in an embryo. Explain what the
advantage is in having this change in position of grey and white matter.
The fetal neural tube is in the middle. The developed medulla oblongata / brainstem region is on the right.
The alar plates have separated laterally and this allows afferent and efferent neurones (grey matter) to
migrate from the inside to the outside of the developing brain. As we move cranially towards the
midbrain, the neural tube closes again and this means that we now have a cortex consisting of grey matter
as well as subcortical grey matter (nuclei). The cortex can now expand considerably by forming sulci and
gyri – increasing surface area without increasing overall size.
Explain what is meant by the “ascending” of the terminal portion of the spinal cord with respect to the
matching vertebral level in the developing embryo, fetus and neonate. You may use a set of well
labelled diagrams as your answer.
- Embryo (around 8 weeks gestation):
- The spinal cord extends the full length of the vertebral canal.
- Each spinal nerve exits at the same vertebral level as its origin from the spinal cord.
- The spinal cord ends at the level of the coccyx.
- Fetus (around 24 weeks gestation):
- The vertebral column grows faster than the spinal cord.
- The caudal (inferior) end of the spinal cord appears to “ascend” and now ends around the S1 (first sacral vertebra) level.
- Neonate (at birth):
- The spinal cord terminates at approximately the L2-L3 level.
- Spinal nerves must now travel obliquely downward to reach their intervertebral foramina.
- Adult:
- The spinal cord usually ends at the lower border of L1 (sometimes L2).
- The cauda equina (bundle of spinal nerve roots) continues inferiorly in the vertebral canal.
Provide definitions for the following neural tube and cranial defects. Spina bidifa occult, meningocele, anencephaly
a. Spina bifida occulta.
(1mark)
Vertebral defect (1/2 mark)
Normal cord and membranes(1/2mark)
b. Meningocele.
(1 mark)
Bony defect with protruding meningeal sac (1/2 mark)
Covered by intact skin (1/2 mark)
c. Anecephaly
(1½ marks)
Cranial vault missing (1/2 mark)
Base of skull malformed (1/2 mark)
Disorganised brain tissue and vessels – cerebrovasulosa (1/2 mark)
Lists three (3) types of cranial embryopathy that is associated with Phenytoin use.
Neural tube defects
Microcephaly
Facial dysmorphism
Outline two (2) characteristics of a good screening test.
Reasonable cost, Easy to perform, Safe and preferably non-invasive, Reproducible results, Must be able to
detect disease early (when it can still be managed), Must be sensitive (must have a low false negative rate)
Outline two (2) indications for prenatal screening.
Answer: Advanced maternal age (>35 yrs); Family history of congenital anomalies (NTD / Chromosome
abnormalities / single gene disorders / other congenital anomalies); Previous child with congenital
anomalies; Abnormalities identified during pregnancy)
Briefly explain the difference in the result that can be obtained from a prenatal screening test and a
prenatal diagnostic test.
A screening test provides a level of risk, but not a definitive diagnosis. A diagnostic test makes a
definitive diagnosis
List two (2) prenatal diagnostic testing options available if NTD screening test is positive.
Amniocentesis; Chorionic villous sampling
Describe the anterior and posterior blood supply to the brain, and how these circuits are connected.
Anterior supply: ICA (½) -> enters cranial cavity through carotid canal (½) -> divides into ACA (½) and
MCA(½)
Posterior supply: Vertebral artery (½) -> joins to form basilar artery (½) -> gives various branches that
supply the posterior brain regions (½).
Anterior and posterior supply connected by the Circle of Willis (½), specifically by the posterior
communicating artery (½) and posterior cerebral arteries (½).
List two (2) ascending and two (2) descending brain tracts. Indicate the type of information each tract
carries.
Ascending (any two of the following):
1. Dorsal columns (½): Proprioception and fine touch (1)
2. Spinothalamic tract (½): pain, temp, course touch, pressure (1)
3. Spinocerebellar tract (½): information from muscle spindles and mechanoreceptors (1)
Descending tracts (any two of the following):
1. Corticospinal (½): Voluntary and skilled movement (1)
2. Rubrospinal (½): Tone of limb flexors (1)
3. Tectospinal (½): mediate reflex movements in response to visual stimuli (1)
4. Vestibulospinal (½): Co-ordinating head and eye movements (1)
5. Reticulospinal (½): Control in breathing and voluntary movement (1)
Describe the anatomy of cranial nerve 5 (CN V). Include in your answer, its origins, its major branches
and the broad regions they innervate, and the types of fibres carried by this cranial nerve.
Origins – Trigeminal Sensory nucleus (½) and Trigeminal Motor nucleus (½)
Branches – (1) Ophthalmic (½) (Scalp, eye, upper face) (½); (2) Maxillary (½) (middle face to tip of nose)
(½), (3) Mandibular (½) (lower face, ant 2/3 tongue, temple) (½)
Fibres – Sensory (½), Motor (½)
List the nuclei that comprise the corpus striatum (1½ marks). For each nucleus provide one anatomical
relation (3 marks). Finally, name the one white matter tract closely associated with the corpus striatum
(½ mark).
Nuclei – Caudate (½), Putamen (½), Globus Pallidus (½)
Anatomical relation – Caudate: lateral wall of anterior horn lateral ventricle (1); Putamen: Lateral to
internal capsule and globus pallidus (1); Globus pallidus: Medial to putamen and the internal capsule (1)
White matter tract: Internal capsule (½)
50a. Name the dural reflection separating the occipital lobes from the cerebellum.
Tentorium cerebellum (½)
Clearly list the names of the layers, in the correct order, of the cerebral cortex compared to the
layers of the cerebellar cortex.
Cerebral cortex: Molecular, External granular, External pyramidal, Internal granular, Internal pyramidal,
Multiform (3 marks)
Cerebellar cortex: Molecular, Purkinje Granular (1½ marks)
- List two (2) causes of intracerebral (intraparenchymal) haemorrhage.
Hypertension (1)
Cerebral amyloid angiopathy (1)
List the two (2) macroscopic types of cerebral infarction and state a cause for each.
Pale (non-haemorrhagic) infarct (1/2)
End-arterial supply (1/2)
Haemorrhagic infarct (1/2)
Reperfusion injury (1/2)
Name the intrinsic property of cortical neurons that gives rise to the pattern of laminar necrosis in
cerebral infarction
Selective vulnerability (1)
State the systemic condition that Charcot-Bouchard microaneurysms are associated with, and outline
the typical microscopic pathology seen in these lesions.
Hypertension (1)
Hyaline arteriolar sclerosis (1)
List two (2) biochemical tests that can confirm the diagnosis. State the direction of change for each
test.Cushings
Any 2 of the following:
a. 24 hour urine cortisol increased
b. Midnight serum or saliva cortisol elevated
c. Loss of diurnal rhythm
d. Low dose dexamethasone test – cortisol not suppressed.
Outline the mechanism for the hypertension in cushings syndrome.
Cortisol is in excess, overriding enzyme that inactivates it (11BHSD – converts cortisol to cortisone) [1],
binds mineralocorticoid receptor [1] increased ENaC channel activity (increased uptake sodium, water)
[1]
State whether the following parameters will be increased, decreased or normal in a patient with
Cushing Disease due to a pituitary adenoma.Cortisol, ACTH
a. Cortisol
increased
b. Adrenocorticotropic hormone
norma/increased
State whether you would offer the granddaughter testing for Factor V Leiden (½ mark). Briefly
explain your answer (1½ marks).
Yes, as she has 2 “modifiable” potential risk factors for DVT if combined with FVL. Not 18 but old
enough to smoke and us OC so likely capable of autonomy
If the granddaughter’s test also shows Factor V Leiden, outline the implications for her father.
Obligate carrier – increased risk of DVT but not inevitable (<5% if no other risk)
