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The enteric nervous system (ENS) or intrinsic nervous system is one of the main divisions of the autonomic nervous system (ANS) and consists of a mesh-like system of neurons that governs the function of the gastrointestinal tract. It is capable of acting independently of the sympathetic and parasympathetic nervous systems, although it may be influenced by them. The ENS is also called the second brain. It is derived from neural crest cells.

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18. Discuss the histophysiology of sight and the visual pathway. Histology lecture in Intro to neuroscience

Visual Pathways = axons of retinal ganglion cells form optic nerve -> medial optic nerve fibres decussate at optic chiasm. Most fibres of optic tract travel to LGB of thalamus and others end in superior colliculi (initiates visual reflexes) and pretectal nuclei (pupillary reflexes and circadian rhythm). Stimulus travels from thalamus to visual cortex (occipital lobe) = for processing of visual information.

The LGB (lateral geniculate nucleus/body) acts as a relay station for visual input en route to visual cortex. It segregates retinal axons in preparation for depth perception and emphasize visual inputs from regions of high cone density and sharpens the contrast info received by the retina.

Occipital cortex = retinopic order = visual field mapped in retina matches to its corresponding regions in visual cortex.

Ocular dominance columns = segregated areas of left and right eye inputs to visual cortex -> preferentially respond to input from one eye or the other.

Cortical processing = primary visual cortex -> process dark/light, colour and contrast.

Visual association areas = form, colour and movement. Anterior to temporal lobe = identification of objects. Parietal cortex and postcentral gyrus = processes spatial location.

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29. Revise the clotting cascade and fibrinolysis. Semester ¾

Clotting cascade = key factors in haemostasis -> bv wall, coagulation factors, platelet plug formation, anticoagulants, fibrinolysis.

Primary haemostasis

Blood vessel wall = endothelium = abruptly constricts following injury and secretes anticoagulation and pro-coagulation molecules.

Platelet plug formation = platelet adhesion, platelet activation and platelet aggregation needed. Platelet adhesion = vWF serves as bridging molecule between GP1b on platelets and subendothelium = this complex exposes binding sites on platelets leads to further aggregation of platelets via vWF and fibrinogen. Platelets activated by collagen + APD + thrombin + adrenalin + thromboxane. Leads to changes in shape of cytoskeleton with contraction of microtubules and synthesis of secondary agonists by thromboxane. Platelets bind fibrinogen and cross link with each other = platelet aggregation.

Secondary haemostasis

Coagulation cascade = fibrin stabilizes and transforms platelet plug into a fibrin reinforced clot. Thrombin is generated and amplified generation then occurs and ultimately fibrin is formed = stabilization.

Cell based model of coagulation = calcium is essential for enzyme-co-factor complex to be maintained on membrane. Commences along extrinsic path on tissue factor bearing cells which complex with factor 7a = TF (tissue factor) – 7a complex which activates factors 9 and 10. Thrombin activates factor 5, 11, 8 and platelets in the intrinsic path.

Factor 9a activates 11 to form 11a. 11a combines with 8a on platelet surface -> leads to common path -> large burst of thrombin production. Factor 13 cross links and stabilizes fibrin polymers therefore platelet plug is strengthened into a fibrin clot.

Inhibitors of clot formation = antithrombin 3, protein C, protein, thrombomodulin and tissue factor pathway inhibitor (TFPI).

Fibrinolysis

Thrombin stimulates endothelial release of tissue plasminogen activator (tPA). Plasminogen-tPA complex binds to lysine site of fibrin clot and tPA cleaves plasminogen forms active plasmin -> dissolves fibrin clot = restores blood flow to the area.

Fibrinolysis is inhibited by plasminogen activator inhibitors (PAI 1 and 2) and by thrombin.

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LO 30 - Revise the structure and function of the pituitary gland. 

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LO 30 - Revise the structure and function of the pituitary gland. 

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22. Compare and contrast grey and white matter. Anatomy lecture in Intro to Neuroscience

Grey vs. White

Grey

• 40% of brain

• All neurons

Its the place where neurons talk and respond i.e. process information

Its like the Facebook chat room

White

• 60% of brain
• Only myelinated and

unmyelinated axons

• It’s the super highways of the brain i.e. connects different parts

• Think of it as fibre optic cable

All brains have grey matter and white matter

3 types of white matter fibres, connecting different parts of white matter in the brain to each other:

• Commissural fibres

Inter-hemispheric communication e.g. corpus callosum

• Association fibres

Intra-hemispheric communication e.g. cingulum

• Projection fibres

Connects different parts of the brain e.g. internal capsule

Also, it is important to note that the grey matter in the brain is the outer cortical layer and the white matter is the inner medullary matter. However, in the spinal cord this is the other way around; the inner substance is grey matter and the white matter is the surrounding/outer layer.

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8. Discuss how strokes affect the cortical/subcortical matter of the brain. AP and Anatomy lecture

Pale infarct = occurs at the end of an arterial territory, the subcortical white matter is expanded and has a pale homogenous and firm appearance.

Haemorrhagic infarcts = caused by a reperfusion of a pale infarct or a superior sagittal sinus thrombosis. The matter below the area of the infarct can also subtly expanded.

Laminar necrosis = not a true infarct, is due to poor perfusion over an area of arterial territory. There is a loss of neurons with the thinning of the cortex. This pattern of injury is usually seen with hypotensive episodes.

Watershed infarcts = wedge shaped infarcts that occur in regions of brain and spinal cord that lie at the most distal fields of arterial perfusion. During these infarcts -> global ischaemia ensues due to hypotension leading to cell death. Often associated with hypotensive episodes, and is often bilateral.

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LO 14

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LO 21 - Discuss cerebral oedema and mass effects. 

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LO 21 - Discuss cerebral oedema and mass effects. 

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LO 07 Describe the autoregulation of blood flow to the brain

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Learning Objective 15- Charcot Bouchard Aneurysms

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Learning Objective 13- Revise the lobes and structures of the brain and their general functions

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Learning Objective 3- Outline cardiac causes of stroke

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Motor representation of the cortex is in the precentral gyrus located in the frontal lobe. Sensory representation of the cortex is in the post central gyrus located in the parietal lobe. The homunculus represents the specific areas of the cerebral cortex in which sensory or motor information is received or transmitted for a certain part of the body. The medial areas of the cortex represent the lower body and trunk and the lateral areas represent the face more.

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A watershed zone is a region that receives dual blood supply branches of two major arteries.

Watershed zones:

Boundary zones between two arterial territories = furtherst away from arterial perfusion,
so drop in pressure affects this area first

Cortical watershed strokes: between cortical territories of anterior, middle and posterior
cerebral arteries. Borderzone between ACA and MCA most at risk.

Internal watershed strokes: in white matter between superficial and deep arterial systems of the MCA or between the superficial systems of the MCA and ACA

The primary watershed area of the spinal cord is the mid thoracic region.

The artery of Adamkiewicz (AKA) branches off the left side of the descending aorta around T8 to L2 (via lumbar or intercostal arteries) and connects on the ventral side of the spinal cord to supply the anterior spinal artery.

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LO 10 - Describe and explain selective vulnerability to CNS hypoxia. 

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LO 10 - Describe and explain selective vulnerability to CNS hypoxia. 

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6. Describe the blood supply to: Anatomy lecture and Anatomy Dissector (Human Biology Practical Workbook)

a) The brain and spinal cord

Arterial supply = internal carotid (80% of brain supply) and forms part of anterior supply of brain. And the vertebral artery = vertebral basilar system supplies the posterior part of the brain. The anterior and posterior supply anastomose in the circle of Willis.

The two anterior cerebral arteries supply motor and sensory cortices for lower limb, and they are connected via the anterior communicating artery.

Middle cerebral artery = supplies the primary motor and sensory cortices for the whole body, except for the lower limb. Also supplies auditory and speech areas.

Posterior circulation = vertebral artery gives off anterior and posterior spinal arteries and posterior inferior cerebellar artery (PICA). 2 vertebral arteries join to form basilar artery.

Basilar artery = gives off AICA anterior inferior cerebellar artery and pontine arteries. Terminal branches = superior cerebellar arteries and posterior cerebral artery.

Posterior cerebral artery supplies occipital lobe and inferior temporal lobe.

Circle of Willis = formed by internal carotid, anterior communicating arteries, anterior cerebral artery, posterior communicating artery and posterior cerebral artery.

Venous drainage = superficial veins = superior cerebral vein -> superior sagittal sinus, superficial middle cerebral veins -> cavernous sinus. Inferior sagittal sinus and great cerebral vein -> straight sinus -> confluence of sinuses -> transverse sinus -> IJV -> SVC. *deep veins drain into internal cerebral veins = which combine form great cerebral vein.

Spinal cord = arterial supply = single anterior spinal artery and paired posterior arteries, radicular artery reinforces blood supply.

Venous drainage = ventral surface -> anterior median and anterolateral spinal veins. Posterior = posterior median and posterior lateral spinal veins. All drain via radicular vein into internal vertebral plexus -> SVC.

Ref: Intro to Neuro lecture : blood supply to the brain

b) The basal nuclei

The arterial supply to the basal ganglia comes mainly from the middle cerebral artery, a continuation of the internal carotid artery.

The main artery is named lenticulostriate artery and, as the name implies, provides most of the circulation to the striatum and the lenticular nucleus.

There is also a small amount of supply from the anterior cerebral artery and the anterior choroidal artery, both of which are also branches of the internal carotid artery, supplying the more anterior aspect of the ganglia, (i.e. the head of the caudate nucleus and the nucleus accumbens). This particularly large artery is referred to as medial striate artery (of Heubner).

The substantia nigra and the subthalamic nucleus are more posterior and thus receive its vasculature from branches of the posterior cerebral and posterior communicating arteries.

The venous drainage is via striate branches of the internal cerebral vein, which drain into the great cerebral vein.

Ref: (Teach Me Anatomy)

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LO 1 and 2

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LO 4 - Aetiology & pathogenesis of Stroke/ TIA

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LO 4 - Aetiology & pathogenesis of Stroke/ TIA

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- Pressure care: The aim is to maintain healthy skin and thus prevent breakdown and the development of pressure ulcers. You will learn about the risk factors that make an individual more susceptible to developing pressure ulcers, changes in skin condition to look out for and how to position individuals to reduce pressure.
- Beta blocker: also known as beta-adrenergic blocking agents, are medications that reduce your blood pressure. Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta blockers cause your heart to beat more slowly and with less force, which lowers blood pressure.
- ACE-inhibitor: a class of medication used primarily for the treatment of high blood pressure and heart failure. They work by causing relaxation of blood vessels as well as a decrease in blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart.

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Mr Errol Petersen, a stressed school principal is now 50 years old, and although he has managed to stop smoking, he has gained weight. He has attended check-ups with his GP regularly since his heart attack two years ago. His blood pressure has been well controlled (145/80 mmHg) since he was prescribed a daily beta-blocker and ACE-inhibitor. He also takes aspirin daily. During a normal working day, he collapses at work and is brought to the hospital unconscious. On examination, he is found to be incontinent with flaccid weakness of the right arm and leg, and upper motor neuron facial weakness. He is breathing normally and maintaining an adequate airway. An ECG confirms the clinical finding of atrial fibrillation. A diagnosis of stroke is made. He is admitted to hospital and is managed with both supportive and pressure care. He is also managed for his urinary incontinence. Over the next few days he recovers consciousness but is unable to speak and appears anxious and frightened, a rehabilitation programme is started and although leg motor function gradually returns, the occupational therapist is pessimistic about his chances of his being able to walk again. He becomes frustrated, uncooperative, moody and difficult to nurse. Mrs Petersen visits every evening with her teenage boys and is increasingly worried about the future, especially because she has been warned that he may never speak again and he is likely to have difficulty performing everyday tasks. She works full time and will be unable to pay for someone to care for Mr Petersen. She feels angry but is reluctant to place Mr Petersen in care, and is considering resigning from work to care for him.Through collaborating well the team of health professionals worked with the Petersen’s to improve Mr Petersen’s functioning and Mrs Petersen’s capacity to support him. Despite this, Mr Petersen struggled to sleep and felt hopeless. The team decided to refer him to a psychiatrist for assessment for possible depression.

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Describe connections and prioritise limitations

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Supportive and Pressure care.
Managed for urinary incontinence
Rehabilitation Programme
Occupational Therapy
Possible referral to a Psychiatrist.
Collaboration of health professional team with Mrs Peterson.

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Diagnosis of a stroke
frustrated, uncooperative, moody and difficult to nurse.

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Incontinent
flaccid weakness of right arm and leg.
UMN facial weakness
Normal breathing
Atrial Fibrillation

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50 year old principal
stressed, stopped smoking
gained weight,
On Beta Blockers, ACE inhibitors. Well controlled blood pressure
Takes daily asprin.
Has a wife and children (Teenage boys)

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Prior Knowledge, interrogate, analyse and identify gaps

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Identify key issues using hybrid SOAP Model

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Read and classify terms