History, Pathology, Physiology Flashcards

0
Q

Where do parasympathetic preganglionic nerve fibres originate?

A

cranio-sacral

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1
Q

Where do sympathetic preganglionic nerve fibres arise?

A

Thoracolumbar

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2
Q

What neurotransmitters are released from preganglionic fibres of sympathetic and parasympathetic nerves?

A

ACh bind nicotinic ACh receptors

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3
Q

What neurotransmitters are released from postganglionic sympathetic and parasympathetic nerve fibres?

A

Sympathetic postganglionic fibres release NA or ACh
Parasympathetic postganglionic fibres release ACh

*ACh binds muscarinic ACh receptors

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4
Q

What are the 2 functional classes of sympathetic ganglion neurons?

A
  • paravertebral ganglia (source of vasoconstrictor neurons)

- prevertebral ganglia (innervate non-vascular smooth muscle)

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5
Q

What are the locations of parasympathetic cranial preganglionic neurons?

A

Edinger-westfal nucleus in midbrain
Salivary nuclei
Dorsal motor nucleus of vagus and nucleus ambiguous

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6
Q

What is white matter?

A

Myelinated axons and glia

Oligodendrocytes give fat the white colour

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7
Q

What is grey matter?

A

Neuron somata, dendrites and glia

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8
Q

What is the appearance of white matter in a T2-weighted image?

A

White matter appears darker than grey matter

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9
Q

What is the anatomical direction of dorsal in the CNS?

A

In brainstem and spinal cord, dorsal is behind

In midbrain, dorsal structures are toward top of head

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10
Q

What splits the cerebral hemispheres?

A

Longitudinal fissure

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11
Q

What divides frontal lobe from parietal lobe?

A

central sulcus

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12
Q

What structure links the left and right hemispheres?

A

corpus callosum

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13
Q

What is the anatomy of the spinal cord?

A

Core is grey matter surrounded by white matter
Dorsal horns - incoming sensory information (ascending pathways)
Ventral horns - outgoing motor information (descending pathways)

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14
Q

Where do the spinal nerves end?

A

Level of L1/2

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15
Q

Where is CSF resorbed?

A

Major veins at arachnoid granulations in the subarachnoid space

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16
Q

What dural petition divides the cerebral hemispheres?

A

Falx cerebri

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17
Q

Which dural petition separates cerebellum from occipital lobes?

A

Tentorium cerebelli

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18
Q

How many closure events of neural tube are there?

Failure of zone closures is associated with what developmental defects?

A

5 independent closure events
failure of zone 5 closure = spina bifida
failure of zone 2 closure = anencephaly

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19
Q

What are the 3 vesicles of the neural tube and what do they form?

A

Prosencephalon - forebrain
Mesencephalon - midbrain
Rhombencehalon - hindbrain

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20
Q

What structures does the prosencephalon split into?

A

Telencephalon and diencephalon

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21
Q

What is the neural crest and what are its derivatives?

A

Cells at the top of the neural tube migrate away from neural tube
Form peripheral NS - DRG, Symp and parasymp ganglia
Melanocytes
Muscle cartilage and bone (skull, jaw, face, pharynx)

22
Q

What is the consequence of no formation of the floor plate?

A

motor neurons don’t form

24
Q

Which cells guide migration in the cortex?

A

Radial glia

25
Q

What cells direct spinal cord development?

A

Notochord

26
Q

What are possible consequences of damage to central axons/neurons?

A
  • neurons die
  • neurons sprout and make new local connections
  • neurons not able to regrow
27
Q

Why are central neurons/axons unable to regenerate?

A

Glial scar inhibits regrowth (oligodendrocytes)

28
Q

What is Wallerian degeneration?

A

degeneration of axon and myelin sheath of peripheral nerve below site of injury
macrophages phagocytose
muscle fibre atrophy

29
Q

What happens 3 weeks post-injury to peripheral nerve?

A

Schwann cells proliferate and form compact cord
growing axons penetrate Schwann cell cord
*Schwann cells support axon regrowth

30
Q

What can happen is peripheral nerves unsuccessfully regenerate?

A

neuroma formation - bundle of nerve fibres which can cause pain or unusual sensations

31
Q

What are mechanisms that inhibit CNS neural regeneration?

A
  • astrocytic gliosis (forms barrier between undamaged tissue and injury site)
  • myelin proteins (Rho signalling inhibits axon growth)
  • upregulation of axon guidance molecules (Rho kinase pathway causes axon to retract)
32
Q

What processes lead to secondary neuronal injury?

A
  • degenerative insults (ischaemia, Ca++ influx, ROS, excititoxicity)
  • immune infiltration and microglial activation
  • inflammatory mediators
33
Q

Where is memory stored?

A

hippocampus in medial temporal lobe

34
Q

How is short-term memory formed?

A

Insertion of AMPA receptors

Enhanced presynaptic release

35
Q

How is long-term memory formed?

A

Protein synthesis

Structural changes

36
Q

What are the 2 main subtypes of cerebral oedema?

A
  • Vasogenic (BBB disruption with increased vascular permeability)
  • Cytotoxic (secondary to injury)
37
Q

What are the 3 sites of herniation?

A
  • subfalcine (under falx cerebri)
  • transtentorial
  • uncal (cerebellum through foramen magnum)
38
Q

What pathological processes are involved in stroke?

A
  • infarction (75%)
  • intracerebral haemorrhage (20%)
  • subarachnoid haemorrhage (5%)
39
Q

What are risk factors for cerebral infarction?

A
  • age
  • hypertension
  • CVD
  • dyslipidaemia
  • DM
  • smoking, obesity
40
Q

What is cerebral infarction?

A

necrosis of cerebral tissue in a particular vascular distribution due to vessel occlusion or systemic hypotension

41
Q

What are mechanisms of cerebral infarction?

A
  • inadequate supply of blood due to pump failure
  • inadequate supply of blood due to narrowed vessel lumen (atherosclerosis, thrombosis, vessel thickening)
  • vessel occlusion by embolus
42
Q

What are cardiac causes of cerebral infarction?

A
  • non-bacterial thrombotic endocarditis (rheumatic fever, hypercoagulable states, abnormal valve formation)
  • probe-patent interatrial septum due to increased RA pressure or abnormal valve formation
43
Q

What is a common site for atherosclerosis?

A

CCA bifurcation

44
Q

What sort of necrosis occurs in the brain?

A

Liquifactive necrosis

Macrophages phagocytose dead tissue which eventually causes cystic changes

45
Q

What is the cause of a lacunar infarct?

A
  • small vessel occlusion leads to small infarct
  • usually due to small vessel disease ad hypertention
  • lacunar infarct can lead to cystic changes
46
Q

What are causes of intracerebral haemorrhage?

A
  • hypertensive small vessel disease
  • cerebral amyloid angiopathy
  • blood disorders
  • tumour
  • drugs
47
Q

What particular sites do hypertensive haemorrages tend to occur?

A
  • basal ganglia and thalamus
  • white matter
  • cerebellum
  • pons
48
Q

What is cerebral amyloid angiopathy?

A

-deposition of A beta amyloid in walls of superficial blood vessels above the tentorium

49
Q

If there are multiple haemorrhage sites in the brain, what is the most likely cause?

A

Coagulopathy issue

Hypertension not likely to cause multiple sites

50
Q

What are causes of subarachnoid haemorrage?

A
  • rupture of berry aneurysm

- extensive intracerebral haemorrage

51
Q

What are risk factors for berry aneurysm formation?

A
  • adult females
  • polycystic kidney disease
  • coarctation of aorta
  • hypertension
  • smoking and alcohol
52
Q

Where do berry aneurysms typically occur?

A

sites of congenital weakness at arterial bifurccations
more likely in anterior circulation
bifurcation site of MCA
junction of ICA and posterior communication artery
anterior communicating artery

53
Q

What are complications of aneurysm rupture?

A
  • subarachnoid haemorrhage
  • cerebral oedema and increased ICP
  • vasospasm and infarction
  • ventricular obstruction (hydrocephalus)
54
Q

What cells induce ventral horn motor neurons?

A

Floor plate