Vivas Flashcards

Question

Describe the research on the current use of C-Collars in the prehospital setting (lecture/tutorial)

Answer 1

Immobilisation / neck collar PRO’s - Stabilisation for extrication - Less secondary injury ( which are less prevelant ) CON’s - Minimal evidence - Vomit = aspiration - Pressure sores = infection - Anxiety

Answer 2

You cannot fully diagnose a SCI but can have very high suspicions, this would include ; - altered sensations on the skin - determine where they lose sensations to what area of the SC is injured - assess through all different sensations (light touch, pain, temperature,) - mechanisms of injury

Answer 3

Autonomic dysreflexia : Medical emergency! This may occurs when a patient has a spinal cord injury below T6 and also needs a compensatory mechanism in place due to an infection or something else. Blocked cathedar : the nerves and neurons below the injury are still functioning but the signals cannot get to the brain. If the cathedar becomes blocked it is sending signals to the brain to compensate but those signals cannot get to the brain hence the continual stretching of the bladder initiates sympathetic stimulation causing blood vessels to constrict and hypertension, The barroreceptors then detect the increase in blood pressure and compensate to decrease HR hence bradycardia. These signals wont be able to reach below the site of injury hence they will continue to be , Vasoconstricted, pale whereas above the injury site will be vasodilated, flushed. We can treat this though removal of the stimuli / infection And decrease the blood pressure to a tolerable range because the blood pressure is really high above the injury this can cause seizures and cerebral haemorrhage therefore reduce blood pressure by GTN but prepare for rebound hypertension and tachycardia Atropine for bradycardia

Answer 4

Prehospital presentation : Response - should not be altered with isolated SCI Airway : may be compromised with injury to C spine Breathing : may be compromised with injury above C3 Circulation : may be compromised due to vasoconstriction or vasodilation - flushed above SCI and pale below - involuntary erection - weakness - effected behaviors / awareness Prehospital Management : - Continually reassess ABC’s - immobilise, Collar, VAC mat - IV access for fluids - atropine for bradycardia - adrenaline infusion for hypotension - oxygen for hypoxia ? - clinical support - early notification - keep then flat and do not move

Answer 5

Is a spinal cord injury caused by herniated disks, direct trauma or malignancy in which causes the paralysis of the tailbone area, faecal incontinence and sciatic pain. An injury to the lower back causing lower back pain

Answer 6

Injury to one’s side of the spinal cord in which results in same side loss of motor, touch and proprioception and loss of pain and temperature on the other side. LEFT SIDE TRAUMA : Pain and temp on right side is lost Motor, touch and proprioception is lost of left side

Answer 7

Injury to the anterior aspect of the spinal cord Caused by ; fractures and dislocations resulting in ischaemia Loss of motor, touch and pain below the injury NO LOSS in touch and proprioception

Answer 8

Incomplete injury to the spinal cord due to cervical / neck hyperextension Upper limb motor weakness and loss of light touch, pain, temp, and pressure below the injury

Answer 9

Complete spinal cord injuries occur when there is complete loss of all functions below the injured site. This may or may not be due to the complete cut of the spinal cord. Incomplete spinal cord injuries are those that still have some function which extends to the S4 and S5 region. Paraplegic – only the lower two limbs are effected quadriplegic – partial or total loss of function of all four limbs

Answer 10

The prehospital management for a spinal cord injury involves the recognition of a SCI with special attention to a thorough secondary assessment, looking for any loss in motor function, touch, temperature, pain and proprioception. From here spinal immobilisation is key, this can be performed through; - manual stabilisation - modified towel role - vac mat - c collar With special mention of the shocked patient - atropine for bradycardia - adrenaline infusion for hypotension - ventilation for hypoxia ? are they hypotensive because they are hypovolemic or do they have a SCI Loss of ANS and SNS tone

Answer 11

PRO’s - Stabilisation - Less secondary injury CON’s - Minimal evidence - Vomit = aspiration - Pressure sores = infection - Anxiety

Answer 12

To prehospital diagnose a patient with a SCI the following should be considered ; - determine what signals are getting through to the peripheries and what are signals are entering the brain Dermatomes (efferent) myotomes (afferent) - Canadian c spine rule / precautions - loss of autonomic nervous system innervation - loss of sympathetic tone and unopposed parasympathetic tone

Answer 13

Meningitis a viral or bacterial infection to the Meningie layers of the brain, dura matter, arachnoid matter and pia matter. When these layers becomes infected they become inflamed and hence increase intracranial pressure. SEPSIS : Bacteria causes the release of endotoxins into the bloodstream ↓ This causes damage to the capillaries and triggers the clotting cascade hence lots of blood clots in the vessels which is depicted as a rash ↓ The body will then run out of the clotting factors ↓ This causes BLEEDING and DIC ↓ DIC causes limb necrosis and damages capillaries The clinical manifestations of meningitis are the triad of; neck stiffness, fever and altered mental state. But can also include; headaches, photophobia and non-blanching rash. Clinical diagnosis for meningitis includes a thorough history and recent infection status and signs and symptoms coherent with the condition as well as vaccination history. Management of meningitis is early identification, PPE, antibiotics for bacterial and antiviral medications for viral, and monitoring of ABC’s with the anticipate to treat shock as this can progress with cardiac arrythmias, hypotension, vasodilation due to the systemic infection.

Answer 14

Is the infection to the grey and white matter of the brain tissue or spinal cord. It can be either viral or bacterial but typically viral is more common as is it smaller hence easier to get to the brain and bacteria is a bigger molecule hence it is harder to get to the brain. This can be caused by herpes, rabies, ebola, ross river, west Nile, covid this viral infection then progress into the brain or spinal cord and hence encephalitis. Cytotoxic – toxic cells ↓ WBC fight back – the white blood cells try to fight the cytotoxins ↓ Inflammation, because the cell are dying and breaking down from the virus ↓ Cerebral oedema from the cell death ↓ Death / long term brain damage from all the cell death Clinical diagnosis for encephalitis includes a thorough history and recent infection status and signs and symptoms coherent with the condition as well as vaccination history. The clinical manifestations of encephalitis include the triad of CNS infections fever, altered conscious state, neck stiffness, headaches, confusion, seizures, personality changes. The management includes early identification and notification, sedation for agitated patient and the preparation for seizures.

Answer 15

Brain Abscess are a bacterial infection caused by the build up of pus and inflamed tissue that builds up due to infections. The pus is a product of bacterial infection and dead white blood cells that have tried to fight the infection. This builds up within the brain and causes large neurological disturbances. This can be caused to a range of bacterial infections dental abscesses, sinus infection ear infections, skull trauma which allows bacteria to enter the brain. The clinical manifestations of a brain abscess include fever, headache, cannot speak, one sided muscle weakness, vomiting and seizures. Change in personality due to the potential in midline shift of the brain, increased ICP as the abscess is growing in a location where there is no space, so all the signs and symptoms that occur when ICP increases. also Increase ICP when laying flat. Clinical diagnosis for a brain abscess includes a thorough history and recent infection status and signs and symptoms coherent with the condition as well as vaccination history. The signs and symptoms will have a gradual onset as the abscess needs time to grow hence will not be a sudden onset. Patient that are higher risk for this infection includes, IV drug users as they use dirty needles potentially with bacteria in then into the veins and those immunocompromised patients. Management will include early identification and notification, symptomatic management, there is minimal interventions we can do prehospitally but antibiotics is key for treatment.

Answer 16

White blood cells fight infections and therefore are needed to help the immune system to fight meningitis, encephalitis and brain abscesses. WBC are located within the bloodstream and therefore when they are required to fight infections in the CNS they cannot diffuse out of the bloodstream. The capillaries need to vasodilation to increase the permeability of the vessel walls hence WBC can exit. This also causes fluid to follow out of the bloodstream. This then causes ; Cerebral oedema ↓ Increased ICP ↓ Compression ↓ Herniation ↓ Death

Answer 17

Paramedics cannot clinically diagnose a common headache or differentiate them from a more serious complication therefore they all need to be treated with high suspicion if they alter from the patients normal perceived headache. The pathophysiology of a headache can be caused by either a primary source such as • Dehydration • Sinus infections • Alcohol • Muscle strain • Anxiety Or a secondary cause or differential diagnosis • Subarachnoid haemorrhage • Cancer • Space occupying lesion • Trauma – skull fractures, concussions • CVA • Meningitis • Temporal arteritis The red flag clinical manifestation of a headache include • Worst / Different / First headache • Speed of onset / Progression • Numbness • “Thunderclap” headache – comes on in a matter of seconds and is commonly associated with an aura (hallucinations) – subarachnoid haemorrhages • LOC / Collapse • Age >50 or <5 • Neuro deficit / weakness, altered sensation, dizziness, • Persistent / recurrent that are getting worse

Answer 18

A migraine differs from a headache in that they have 4 phases Their population group is usually boys before puberty, girls after puberty and is thought to be strongly related with hormonal changes (hence decrease with pregnancy, after menopause and boys post puberty) Phase 1 : Prodromal phase - this is where the patient will feel the migraine coming on and experience a wide presentation including depression or euphoria, heightened sensitivity to smells and sounds, food cravings, muscle aches and GI upsets. This onset my range from days to weeks before the onset of phase 2 Phase 2 : Aura phase – this is the warning sign that the migraine is about to occur and this can present as visual disturbances, sensory issues like numbness and tingling, motor deficits such as loss of proprioception and balances. This typically lasts an hour before the onset of phase 3. Phase 3 : Pain phase – this is the head pain itself, unilateral head pain on one side and pressure behind the ear, throbbing and intense pain. Can also present with photophobia and phonophobia, neck stiffness, nausea and vomiting and diaphoresis. This phase typically lasts 12 – 24 hours before the onset of phase 4 Phase 4 : Postdromal phase – this is when the pain has ended and the patient is returning to their normal self. This may include depression / euphoria, fatigue, cognitive deficits and confusion, GI symptoms. The migraine is typically unilateral with a throbbing and pulsating pain, it can be triggered by a range of cause • Stress / anxiety • Hormonal changes • Environmental factors (bring lights, strong smells) The treatment for migraine differ with each patient therefore whatever worked last time try again and if it didn’t work try something new. There are a range of medication that can help with migraines • Triptans - serotonin agonist (specific to migraines) • Topiramate - antiepileptic • Sodium valproate - antiepileptic But the most effective treatment for paramedics is to remove the stimuli and reduce light and sounds, NSAID and IV fluids for dehydration and vasodilation to improve perfusion as migraines may decrease blood volume and cause vasoconstriction. Opioid medication are not to be given to migraine patients as they have been shown to increase the intensity of the migraines. Rather begin with paracetamol and ibuprofen.

Answer 19

As prehospital clinicians without access to medical imaging it is difficult to assess the internal working of a patient especially the brain therefore patients that present with abnormal headaches or migraines may have an underlying cause that cannot be determined prehospitally. If the patient presents with any of the below red flag symptoms they require hospital investigation. • Worst / Different / First headache • Speed of onset / different progression • Numbness • “Thunderclap” headache – comes on in a matter of seconds and is commonly associated with an aura (hallucinations) that can be indicative of a subarachnoid haemorrhages • LOC / Collapse • Age >50 or <5 • Neuro deficit / weakness, altered sensation, dizziness, • Persistent / recurrent that are getting worse • Stiff neck, photophobia and vomiting = cerebral bleed or meningitis until proven otherwise Although headaches may cause an ambulance to ramp for many hours it is better the be safe than to be sorry and leave a patient home with what presents as a typical gradual onset headache that may be a brain abscess. The only time paramedics can leave a patient with a migraine home are if the cause of the migraine is known to the patient and there is a simple fix ie the patient ran out of migraine medication and is yet to fill their script. ECP may be able to administer medication with the agreement that if the migraine develops that they call an ambulance immediately.

Answer 20

Hydrocephalus is the abnormal build up of CSF within the ventricles of the brain. There are four different types : 1. communicating hydrocephalus : where the brain has issues with the reabsorption of CFS hence it builds up (subarachnoid haemorrhage) 2. obstructive hydrocephalus : where there is a blockage in the ventricular system preventing CSF to flow freely (tumours) 3. normal pressure hydrocephalus : this is when CS causes ventricle enlargement without increasing ICP and commonly presents with cognitive dysfunction and urinary incontinent. 4. hydrocephalus ex vacuo : is due to brain atrophy causing the ventricles to enlarge and hence increasing the demand for CSF. (Alzheimer’s disease or post stroke) Signs and symptoms : Infants – • Enlarged head : rapidly increase head size or a visibly swollen fontanelle • Bulging fontanelle : may appear tense or bulging • Irritability : increased fussiness or crying • Poor feeding and poor appetite • Lethargy • Developmental delays : not hitting correct milestones Children and adults - • Headaches : worsen in the morning and after laying down • Nausea and vomiting : • Blurred or double vision : • Balance problems • Cognitive changes : memory problems, difficulty concentration, changes in personality Older adults – • Difficulty walking or feeling unsteady • Cognitive decline : memory loss, confusion, changes in personality • Urinary symptoms : increased urgency or incontinence And in all ages cushing triad – Late stage - Hypertension : The body attempts to maintain cerebral perfusion despite elevated intracranial pressure. - Bradycardia : Increased ICP can stimulate the vagus nerve, leading to a reflex bradycardia as a compensatory response. - Chain stokes respirations : Increased pressure on the brainstem can disrupt normal respiratory control centres. There’s nothing we can do prehospitally but in hospital they can put shunts in to allow the drainage of CSF into the abdomen When CFS leaks from the ears and nose this means that their meninges layers have broken

Answer 21

Bacteria, virus, parasite, fungi The microbe needs a temporary place to reside before infecting the patient this may be in waterways or animals. There is then a mode on transmission / how the microbe gets onto out body this can be through the consumption of the animal or water, bites or scratches from the animal, through droplets like sneezing and poor hygiene. The microbe is then on and can enter it through a portal either eyes, nose, ears, mouth, wounds, genitals, skin – some worms can enter the body by burrowing in via the skin. The white blood cells then begin to fight the infection this can either successful or unsuccessful due to autoimmune diseases, elderly or newborns. The microbes then colon on the host which in us and it claims our body as their new home.

Answer 22

Viruses are innate hence they need a host to thrive whereas bacteria their own living organism. Bacteria replicated itself with food and fuel hence keep multiplying whereas viruses have their own DNA and RNA hence they replicate without a biological process. Virus destroy cells by damaging the phospholipid membrane and taking all the cells energy then jumping to the next cell and doing the same, whereas bacteria can kill cells though the release of toxins and invading the host cell.

Answer 23

The guidelines address status epilepticus by : 1. vascular access ? YES – administer IV / IO midazolam 0.15mg / kg (max 10mg) NO – IM midazolam 0.15mg/kg OR IN / buccal 0.3mg/kg 2. IV / IO administer IV / IO midazolam 0.15mg / kg (max 10mg) 3. Seek ICP help 4. Confirm status epilepticus seizure administer levetiracetam or phenytoin 5. Give the opposite to what was given before either levetiracetam or phenytoin OR phenobarbitone 6. Call for MedStar and RSI (intubation) The differences between SAAS guidelines and APLS guidelines is that they suggest to administer 0.15mg/kg and SAAS gives 0.1mg/kg.

Answer 24

The children at risk for febrile convulsions are children ages 6 months to 5 years of age with the main population being 12 – 18 months and more common in females. The pathophysiology for febrile convulsions are unknown but they were thought to have been from the rapid spike in temperature of above 38 degrees as well as the immature brain unable to thermoregulate as effectively as the adult body therefore are more predisposed to febrile convulsions. The prehospital treatment for febrile convulsions are to address the root cause of increased temperature therefore removing the peads clothing and applying cool packs on the appropriate areas, arm pits, neck and groin to decrease temperature. Oxygen therapy and glucose for the cerebral hypoxia. And monitor ABCS. If the seizure has lasted longer than 5 mins or the patient has not returned to their normal GCS during their post ictal phase then administer 0.1mg/kg of midazolam and follow status epilepticus protocols

Answer 25

The key clinical features of a pead may include but are not limited to - Vomiting - Irritability - Altered consciousness - Bulging Fontanelle / whole head enlargements - Sunset pupils / unreactive or not symmetrical pupils - Cushing triad o Bradycardia o Hypertension o Irregular respirations ( Cheyne Stokes )

Answer 26

The paediatric GCS scale is a modification from the adults scale with adjustments to the voice aspect, it is altered to 5 : alert and uses words as normal 4 : less words than usual, spontaneous crying 3 : crying to pain 2 : moans to pain and 1 : is no response. Whereas the AVPU scale is an initial rapid assessment that determines the consciousness of your paediatric patient. A : Alert V : Alert to voice P : Alert to pain U : unconscious AVPU is faster but GCS is more through and detailed therefore it is preferred to use AVPU initially then progress to GCS.

Answer 27

Acute delirium is an acute change in mental status where the patient is not in touch with reality. It has a sudden onset and can be reversed / treated hence how it differs from dementia as this is a progressive onset over years and has no cure. Clinical manifestations : - not in touch with reality - acting unusual - paranoid - confused - agitated Why may this occur : - infections (UTI) / sepsis - cerebral hypoxia - new medications / dosing - head trauma - dehydration

Answer 28

Pathophysiology : Parkinson’s disease is a result of damage to the cells within the midbrain that synthesise dopamine therefore there is no release in dopamine. As dopamine is essential for motor skill the patient will present with tremors, slowed movements, rigidity. This can arise form environmental factors or genetic predisposition There is no cure for Parkinson’s disease but there are treatments that can slow its progression and increase a patients quality of life. Parkinson’s disease is also linked closely with Lewy body dementia where there is a depletion of dementia as well as some other cognitive dysfunctions.

Answer 29

Acute behavioural disturbance in elderly can be caused by infectious agents ranging from minor skin infections to sepsis. This alters their cognition and normal levels, may make them agitate and aggressive but it is due to the underlying medical problems.

Answer 30

Is an umbrella term that describes a collection of symptoms that are caused by disorders affecting the cognitive function. Dementia affects thinking, behaviour and the ability to perform everyday tasks. Where its progression is severe enough to interfere with the person’s normal social or working life. The most common types of dementia are • Alzheimer’s disease • Vascular dementia • Lewy body disease • Frontotemporal dementia

Answer 31

In a typical brain amyloid prosecutor protein (APP) is broken down into soluble fibres by alpha and gamma secretase but in the presence of beta secretase the APP becomes insoluble and therefore when binding with other insoluble APP clumps creates a beta amyloid plaque. These plaques can continually develop and are typically situated between the neurons and disrupt neuron signalling and can create an inflammatory response damaging surrounding neurons. These beta amyloid plaque can also situate themselves upon the blood vessels within the brain making the vessel wall thinner increasing the risk of intracranial haemorrhage.

Answer 32

neurofibrillary tangles which are subject to the increase in phosphate groups binding to the microtubules changes structure if the tau, therefore inhibiting its binding ability and creating large tangles of tau. The removal of tau from the microtubules means that they can no longer transfer messages which results in disrupt neuronal signalling and can progress to apoptosis of neural cells.

Answer 33

Alzheimer disease is one of the most prominent types of dementia, it occurs due to the formation of amyloid plaque and neurofibrillary tangles. It can be due to genetic predisposition or sporadic onset. In conjunction with neurofibrillary tangles and the build up of beta amyloid plaque the brain undergoes atrophy where the cerebral cortex shrinks, the ventricles enlargen and the hippocampus shrinks as well as neuronal cell death due to the healthily neurons losing their ability to function and process information all attributing to the clinical symptoms of - Memory loss - Disorientation to time and place - Changes in mood / behaviour and personality - Declines in judgement

Answer 34

inhibit the reuptake of norepinephrine and serotonin by blocking the transporters responsible for their reabsorption into presynaptic neurons. This results in increased concentrations of these neurotransmitters in the synaptic cleft, enhancing their availability to bind to postsynaptic receptors. Therefore, enhancing mood and alleviating depressive symptoms. As this medication inhibits the reuptake of serotonin when patients overdose on these medications it causes serotonin syndrome which is when there is too much serotonin in the synapse this causes muscle spasms and hyperreflexia. As well as this TCAs can block cardiac sodium channels, leading to prolonged depolarization and slowing of cardiac conduction. This can cause arrhythmias, conduction delays (like QRS widening), and potentially lead to ventricular tachycardia or fibrillation. The management of this anticholinergic overdose includes the administration of Activated Charcoal which will absorb the toxins within the body and prevent them from entering into the bloodstream, but also managing symptoms and preparing for patient deterioration and seizure management. Therefore the clinical signs and symptoms would correlate with those anticholinergic toxicity which includes - Dry - Hot flushed skin - Urinary retention - Confusion / delirium - Tachycardia - Hypotension Which leads to - Hyperthermia - Seizures - Dysarrythmias

Answer 35

Typical antipsychotic medications are those that are antagonists to the D2 receptor which means that they block the binding of dopamine on three pathways (mesolimbic, nigrostriatal, mesocortical) and therefore the body compensates to this blockage and decreases the amount of dopamine that is synthesised. In relation to psychosis these medication create a more neurochemically balanced environment for the brain therefore decreasing the episodes of psychosis as the brain is more balanced with its neurotransmitters. These antipsychotics are indicated for patients with schizophrenia and acute psychotic outbursts but can also be used as a second line treatment for nausea and vomiting particularly in chemo patients. - Haloperidol and droperidol are both very common FGA’s

Answer 36

Atypical antipsychotics work on D2 receptors but also histamine, serotonin and alpha receptors. They work the same as first gen but have a higher affinity to the histamine, serotonin and alpha receptors hence their multi-receptor action allowing them to address a larger range of symptoms associated with psychotic disorders. They also have less side effects than first gen hence they are used more often within the community. They are indicated for schizophrenia, bipolar disorders and depressive disorders. Some common community second gen antipsychotics - Olanzapine

Answer 37

Benzodiazepines bind to GABA A receptors which open the ion gated channels and allow the influx of chloride into the neuron. This hyperpolarises the neuron hence it becomes more negative and decreases the neural firing as there needs to be a larger stimuli to create an action potential. From this hyperpolarisation the sedative symptoms arise as there are reduced amount of neural signalling the patient becomes sedated therefore benzodiazepines are indicated for patient who require sedation and patients with increased anxiety. The common ones are diazepam and lorazepam

Answer 38

Cholinergic medications are those that enhance the effects of ACh therefore within a cholinergic overdose there is too much ACh within the synaptic cleft as the AChE (the enzyme the breaks down ACh) is inhibited and therefore ACh cannot be reuptake into the synapse. These overdoses are generally organophosphate poisoning. These patients will present with ; S – salivation L – lacrimation (crying) U – urination D – defecation (pooing) G – GI disturbance E – emesis (vomiting) B – bradycardia B – bronchoconstriction B – behavioural disturbances The management for these patients are supporting their ABC’s and intervening as necessary. The antidote for this is atropine it works by binding to the M2 receptors therefore stopping the excessive amounts of ACh binding to these M2 receptors. Typically ACh slows heart rate by reducing the firing rate if the SA node, therefore excessive ACh will induce bradycardia but when administering atropine it will block the M2 receptors and also reduces parasympathetic / vagal tone hence allow the rise in heart rate.

Answer 39

Anticholinergic medications that block ACh from binding to muscarinic receptors, as well as inhibit this signalling pathway. This means that there is not enough ACh within the synapse / body and therefore stopping the depolarisation of neurons hence the next neuron won’t get the message leading to a reduced cellular response. These overdoses are typically from pharmaceutical medications like antihistamines this will present with symptoms as following; - dry mouth - urinary retention - flushed skin - tachycardia - hypertension - confusion and agitation these symptoms can all lead to; - dysrhythmias within the heart due to the loss of vagal tone, - seizures due to the reduced ACh and imbalance of excitatory and inhibitory neurotransmitters - hyperthermia due to the body decreased ability to sweat as the muscarinic receptors within the sweat glands are blocked as well as vasodilatory effects reducing ones ability to temperature control. The management for these patients include the administration of activated charcoal if the anticholinergic was ingested and the patient is alert. Activated charcoal has a very large surface area therefore when ingested also it absorbs the all the toxic molecules GI tract therefore reducing the amount of anticholinergic agents within the systemic circulation therefore decreasing the severity of the symptoms.

Answer 40

Cerebral palsy describes a group of permanent disorders that is caused by damage of injury to the foetal or infants brain hence is not progressive. This causes disruptions in the brains motor pathways leading to abnormalities in movement and posture causing limitations in activities. The clinical manifestations of one with cerebral palsy is dependant of their severity therefore can present with minimal symptoms such as behavioural disorders, salivation issues, speech and sleep disturbances, unable to walk and talk and having an intellectual disability and or epilepsy. The diagnosis for one with cerebral palsy is muscle strength tests, blood and lab testing, history and neurological imaging to determine the extent of the injuries. But most is depicted through their physical and neurological testing. Prehospital management for this patient group is determining their baseline through family communications and treat their presenting complaint. Also as these patients are not in control / lack muscle movement we need to be very cautious of their airway and uncontrolled salivation as they may begin to aspirate on their saliva if their airway is not well maintained.

Answer 41

MS is an autoimmune neuromuscular disorder characterised through the sclerosis of glial cells. This occurs when an unknow stimuli immune response initiates T cells to activate macrophages and b cells to attack the glial cells (Schwann cells and oligodendrocytes) and myelin sheaths therefore inducing sclerosis of the myelin sheaths and slowing down the propagation of the signal. The optic nerve is particularly vulnerable due to its size and location degeneration to this nerve can induce vertigo and involuntary eye movement and issues with vision therefore for some patient this will be one of the first signs and symptoms. This disrupts in signalling pathway from the brain to the muscles therefore patients will typically present with increased fatigue, motor impairments: weakness, spasticity, or coordination problems, sensory changes: numbness, tingling, or pain, vision problems, cognitive changes and emotional changes. The diagnosis criteria for MS includes medical imaging and CSF testing for specific biomarkers that indicated myelin sheath deterioration. Prehospital management for this patient group is determining their baseline through family communications to determine if they are potentially deteriorating and treat their presenting complaint, along with their symptoms.

Answer 42

MND is the progressive degeneration of upper and lower motor neurons where the where the immune system attacks the neurons within the brain due to an unknow reason, yet to be discovered. It differentiates from MS as this attacks the actual neuron itself rather than just the myelin sheaths. This attack can be isolated to upper neurons which cause spastic contractions of muscles or lower neurons which means that the messages can’t send to the muscles hence if we don’t use the muscles they become weak and begin to die. In the beginning MND manifests as muscle weakness to the progressive point of paralysis but can depend on the person and the disease progression and intense but typically from onset patient have between 1 – 5 years left to live. The average age in which people are diagnosed with MND is between 45-60 y/o with the cause still to be determines although it is thought to be due to a range of environmental and genetic factors.

Answer 43

Huntington’s disease is a progressive neuromuscular disease that involves a mutation to the Huntington gene which causes the CAG codon becomes overexpressed hence to misfold and aggregate disrupting cellular functions. This gene disturbance causes a wide-spread loss of neurons and cell death of the basal ganglia and cerebral cortex which are involved in the control of movement, cognition and sensory pathways. This damage reduces the synthesis and release of GABA, this then increases the stimulation of glutamate while also increasing the in dopamine signalling. This dysfunction of the basal ganglia and the imbalance in neurotransmitters causes involuntary muscle control. The increase in inhibitory neurotransmitter GABA and glutamate enhance the release if dopamine therefore there is complications with cognitive decline and mood disorders. The severity of Huntington’s disease can have alternate profiles of 1. cognitive : which describes all the characteristic within the brain damage, memory loss, problem solving, decision making, learning and concentration. 2. motor profile : is subjective to balance, coordination, movement, speech and swallowing 3. psychiatric profile : is characterised by their changes in behaviour, mood, anxiety, depression and psychosis. The clinical manifestations of huntingtins disease align with their profiles therefore can present with three different and each differ in the severity. Our management for these patients includes symptomatic treatment, and behavioural concerns. These patients may also have issues with swallowing and salivation therefore we need to be cautious of their airway and the increased risk of them aspirating on their saliva.

Answer 44

Guillain-Barre syndrome is the paralysis caused by a previous infection which triggers an autoimmune attack which triggers the release of pro-inflammatory cytokines that contribute to nerve damage and exacerbate the inflammatory response hence attacking the peripheral nerve fibres. and therefore depending of the severity depends on the progression of paralysis. The exact pathophysiology and reasoning behind GBS is unknown but it is thought to be from this cause. The clinical manifestations of GBS begin with numbness and tingling within the toes and fingers then progress to full over either hours or days. There is typically a source of infection prior which triggers the paralysis. This paralysis can be reversed with the correct treatment in a timely manner and the patient will then make a full recovery. Our management is recognition that the patient may have GBS and rapid transport to RAH for further investigation and testing via lumbar puncture to either diagnose or rule out other syndromes.

Answer 45

- Chain stokes breathing - widened pulse pressure - pupil changes - hypertension -> hypotension - Tachycardia -> bradycardia - change in mental state - seizures due to the abnormal electrical activity - nausea and vomiting due to stimulation of the medullary vomiting centre - mechanism of injury - tissue swelling - cerebral hypoxia - haemorrhage - increased ICP

Answer 46

The main risk factor when attending to elderly patients is the risk of intracranial bleeds due to their anatomy and potential medications. In the coroners report it states that for every elderly patient on anticoagulant medications they are required to attend hospital for medical imaging. This is to rule out any brain bleeds or injuries. They are at increased risk of brain bleeds due to the anticoagulant medication which slow down clotting therefore reducing fibrin formation and preventing clots from forming. Anti platelets prevent platelets from clumping together and also prevent clots from forming. Elderly populations are typically on these medications to prevent CVA’s but increase their risk for brain bleeds. As well as this elderly patient have brain atrophy and therefore can mask symptoms as there is increased space within the brain for it to bleed in.

Answer 47

A SDM is a person that the incapacitated person has delegated to be the primary decision maker about your future health care, end of life, living arrangements and other personal matters in coordination of your Advance Care Directive. This person will only come into play when you are unable to make health decisions for yourself whether for a short time only, or permanently. This person is only in use for a short period of time or permanently. They make decision in coordination with your ACD but is able to be overruled by the POA. A power of attorney has different levels either General POA or Enduring POA A general power of attorney is someone that you give power to act on your behalf through personal, medical and financial aspects. This power typically is in use when the sick person becomes incapacitated and therefore the GOPA begins to make decisions for the incapacitated person. An EPOA is someone that continues to operate after your death where the take care of personal, medical and financial aspects ie selling cars and houses. You can't make a power of attorney after you have become legally incapacitated but you can cancel your enduring power of attorney at any time, as long as you still have legal capacity. Both POA can trump the decisions of the SDM.

Answer 48

The ACD upholds the principle of patient autonomy, allowing individuals to make decisions about their own medical care in advance for when they becomes incapacitated. This means that the patient knew what they were writing and their wishes for when they become incapacitated. The ACD can never be challenged by paramedics as this is a legal document in which the patient has stated their wishes before they have become incapacitated. The only time paramedics cannot follow it is if the ACD is out of date or not legally correct (isn’t a formal document)

Answer 49

When the patient becomes legally incapacitated. They need to fail either one of the capacity questions then paramedics have a duty of care to the patient and can take them to hospital. in coordination with this we need to address the ACD and be in contact with either the SDM, POA or a responsible person if none of these is available then we have a duty of care to the patient and by calling the medical director or patients GP we can take them to hospital without their consent. Also initiating treatment to a child against the parents’ wishes if the treatment is life sustaining and in the best interest if the child’s health and wellbeing, paramedics can go against the parents’ wishes.

Answer 50

If the person is not capable for the following then they do not have capacity. 1. Understand the information : this means that you need to explain medically what is worrying you and why they need to go to hosptial, without medical jargon and bias, clearly in a way the patient can understand. 2. Retain the information : have the patient re-explain what you have said previously for evidence of good congnition. 3. Using the information to make a sound clinical decision : the patient needs to be able to understand the medical consequences of staying at home and cannot be influenced by other daily activities, bowels of shopping. 4. Communicating : the patient needs to communicate their wishes to you in a way that is best for the patient, voice, sign language or writing notes. If the patient fails to complete one of these tasks they are not capable of capacity and therefore paramedics are able to take them to hospital under our duty of care.

Answer 51

Cerebral autoregulation is the process in which a patient can adequately perfuse their brain by inducing vasodilation and vasoconstriction where appropriate for optimal perfusion for function. By inducing these behaviours it can either increase (vasodilate) or decrease (vasoconstrict) the amount of blood and therefore BP, oxygen and glucose in which enters the brain. When this autoregulation becomes inhibited due to an inadequate MAP outside of 50 - 150 mmHg because of sepsis, hypovolemia, heart issues and hyper / o / tension. When MAP goes out of its range below 50 mmHg the arteries dilate to a point of collapse and opposingly when the MAP is too high the arteries vasoconstriction to a point of max constriction. Then the brain looses its capacity to vasoconstrict. MAP = 1/3 pulse pressure + diastolic BP CPP = MAP - ICP We aim for a MAP of 90mmHg and a cerebral perfusion pressure of 75mmoL

Answer 52

The clinical diagnosis for a TBI include - ROSIER - GCS under 8 - mechanism of injury - declining observations especially neuro obs : declining GCS, pupil changes (unequal and then dinner plates), chain stokes breathing, widening pulse pressure, tachy then extremes Brady. - the diastolic wont always change but the systolic always goes up The management for a TBI includes 1. Avoid hypoxia, hypotension and hypoglycaemia (give oxygen, fluids, and glucose if indicated) 2. Posture the head 30 degrees to allow for venous drainage and blood volume in the brain to decrease. 3. Administer fluids to achieve a MAP of 90 or a systolic BP of 120mmHg. 4. 20 max scene time 5. Avoid seizure and vomiting as this will increase ICP and make the patient deteriorate

Answer 53

Monro–Kellie doctrine is a relationship between blood, CSF and brain tissue within the skull when these are all balanced the brain is able to function appropriately and maintain a normal ICP of 5 - 15 mmHg. In the circumstances of a TBI the brain becomes herniated and the increase in ICP and brain swelling causes abnormalities and tissue damage at the RAS, this is why there is a sudden drop in GCS and cardiac and respiratory changes as the brain stems controls these mechanisms. This can be evident as ICP increases the CSF beings to displace and leak through the Forman Magnum and the progresses to blood then brain tissue. For CSF to leak from the other cavity of the face, eyes, nose, ears the meningial layers need to be broken.

Answer 54

A primary brain injury is the immediate damage to brain tissue and surrounding structures caused by an external force. This can be from a blunt trauma such as hitting your head causing damage like skull fractures, base of skull fractures and concussions which is described as an alteration in cerebral function without structural defect that manifests as a LOC followed by a rapid recovery. Within a concussion there must be 1. LOC 2. RAS disruption, unconsciousness or seizure 3. Acceleration / deceleration injuries where the brain has been smashed against the front of the skull then the back due to the mechanism of injury. 4. Signs and symptoms : light-headedness, vertigo, headaches, nausea, vomiting, photophobia, fatigue A secondary head injury is damaged cause after the injury due to intracranial or extracranial causes Extracranial causes are those that are outside the brain - Hypoxia - Hypoglycaemia Intracranial causes are those which occur inside the brain - Haemorrhage - Swelling - Infections Therefore pathophysiologically they have different mechanisms of action and create different presentations in our patients. But all come together to cause significant damage to the brain tissues and cerebral functions.

Answer 55

The prehospital management for a patient who has suffered a SCI includes - the identification of a potential SCI this may include any of the c-spine precautions. LOC, back / neck pain, distracting injuries, reduced GCS, new motor sensory deficits, previous history of spinal disease or injury. - DRCACBC : ensure that these are all monitored during the progression of the case - immobilise patient to reduce further risk of injury, collar, vac mat, towel roll - IV access - early notification and clinical support A patient with a high spinal cord injury may develop neurogenic shock due to the dysregulation of the autonomic nervous system, this loss in sympathetic tone and unopposed parasympathetic tines below the injury may lead to hypotension, bradycardia and temperature dysregulation. Early identification and aggressive treatment is required to further prevent secondary injuries. In regards to the shocked patient the following would occur; Hypoxia : oxygen therapy with ETCO2 attached - can be titrated Severe hypoxia : BVM with 100% oxygen or intubation Hypotension - give fluid therapy sodium chloride 0.9% 50ml blouses or to effect Severe hypotension - adrenaline infusion with IV fluids Aims to maintain a MAP of 80mmHg Bradycardia - atropine to increase parasympathetic innervation Severe bradycardia - external cardiac pacing

Answer 56

Atropine is used for cases of bradycardia, it is an anticholinergic agent, meaning it blocks the action of acetylcholine (ACh) at muscarinic receptors in the body. It competitively binds to the muscarinic receptors on the heart and smooth muscles to prevent ACh from binding and therefore increases potassium within the cell hyperpolarising the cell making it more negative and harder to depolarise. It promotes muscle contractions and therefore increases heart contractility by increasing the stimulation of the AV node

Answer 57

The nexus criteria assesses a patient to determine of the need radiography imaging. The patient needs to be able to complete the following in order to be c sine cleared; 1. No C spine tenderness 2. Not intoxicated 3. Normal GCS 4. No focal neurological deficits 5. No distracting injuries This guide is a great screening tool but not a diagnostic tool therefore these patient should be treated with caution and with high suspicion. The Canadian c spine rule is another more in depth way to assess a patient for a c-spine injury. This categorises patients that are in the high risk, low risk and no c spine category The high risk factors - over 65 years - dangerous mechanisms - parathesias in extremities Low risk : - simple rear end - ambulatory at any time - delayed onset of neck pain - absence of c spine tenderness Are they able to rotate their neck 35 degrees both left and right without pain.

Answer 58

The current research on c-collars is controversial, some paramedics like to utilise this device as it keeps them free for other interventions and some paramedics dislike the device as they think that is does more harm than good. The pros for the c-collar ; - stabilisation of the c spine to prevent further secondary injuries - remind the patient not to move their head / neck The cons for the c-collar ; - minimal evidence for its effectiveness - risk of vomiting and aspirations - pressure sores leading to infections - its not a very comfortable device and may include patient anxiety.

Answer 59

The diagnosis prehospitally is minimal as we don’t have medical imaging but we can be highly suspicious of SCI. This would include but is not limited to determining what signals can get to the brain and which signals cannot, this means that there may be alterations to dermatome and myotome function. We can also determine where the SCI is by what the functions the body is still able to uphold. Dermatome function : This is the afferent signals that go from the skin into the CNS. To determine at what locations the SCI has occurred the patient will lose the ability to define sensations such as fine touch, but may come across as tingly, sharp, dull or can’t feel. This should be repeated various times to evaluate further progression. The patients can progress negatively due to tissue hypoxia, hypertension and swelling effecting the transmission of impulses. Myotomes are the efferent signals that leave the brain and send signals to the muscles and glands to initiate an action. Myotome function can be tested through muscle strength and coordination of actions. Both myotomes and dermatomes deficits can occur in a patient with SCI or they can have one or another it depends of the mechanisms of action and the injury itself, it may only be an incomplete SCI of the patient only has one deficits either myotomes or dermatome. The use of the Canadian C-spine criteria and nexus criteria are also helpful when determining if a patient has sustained a SCI and if they are requiring c-spine precautions and medical imaging.

Answer 60

Patients who have a SCI are at an increased risk of acute and chronic complications, the acute complications include - the risk of vomiting and aspirating due to their immobility - temperature regulation due to down regulation of the autonomic nervous system - loss in respiratory and cardiovascular capacity And more chronic complications include but are dependant on the level of injury - paralysis either paraplegic (only arms or only legs) and quadriplegic (arms and legs) - DVT and pressure sores due to immobility - Autonomic Dysreflexia : this is when a patient has a SCI above the level of T6 and an acute infection below the site of injury. For example they have an injury at or above T6 and a blockage in their urinary catheter, this means that the bladder can no longer secrete urine which leads it to becoming very full and stretched. The stretch in bladder sends signals to the brain via the spinal cord. When the impulses reach T6 the sympathetic neurons induce vasoconstriction to increase the blood pressure. The rise in blood pressure is detected by the baroreceptors and send signals to the brain to decrease blood pressure, the brain then send messages via the vagus nerve to slow the HR and therefore reduce blood pressure then sends a message down the spinal cord to vasodilate the blood vessels but because of the injury the message does not get passed T6 and therefore only the vessels above T6 are dilated the rest are still constricted hence the blood pressure continues to rise. That’s why these patients present flushed above the injury side and pale below bradycardic. The treatment for autonomic dysreflexia includes the prevention of seizures and strokes due to the hypertensive patient. 1. Identify and address simple reversible causes of stimuli hence remove the stimulus (flush / unblock catheter ) 2. If hypertension persists and no neurological symptoms of stroke are present, administer GTN 400 microgram sublingual, every 5 minutes until symptoms subside and be prepared for rebound hypertension and tachycardia.

Answer 61

this is when a patient has a SCI above the level of T6 and an acute infection below the site of injury. For example they have an injury at or above T6 and a blockage in their urinary catheter, this means that the bladder can no longer secrete urine which leads it to becoming very full and stretched. The stretch in bladder sends signals to the brain via the spinal cord. When the impulses reach T6 the sympathetic neurons induce vasoconstriction to increase the blood pressure. The rise in blood pressure is detected by the baroreceptors and send signals to the brain to decrease blood pressure, the brain then send messages via the vagus nerve to slow the HR and therefore reduce blood pressure then sends a message down the spinal cord to vasodilate the blood vessels but because of the injury the message does not get passed T6 and therefore only the vessels above T6 are dilated the rest are still constricted hence the blood pressure continues to rise. That’s why these patients present flushed above the injury side and pale below bradycardic. The treatment for autonomic dysreflexia includes the prevention of seizures and strokes due to the hypertensive patient. 1. Identify and address simple reversible causes of stimuli hence remove the stimulus (flush / unblock catheter ) 2. If hypertension persists and no neurological symptoms of stroke are present, administer GTN 400 microgram sublingual, every 5 minutes until symptoms subside and be prepared for rebound hypertension and tachycardia.

Answer 62

There are 4 common syndromes that can arise from a SCI these include - central cord which the result from incomplete SCI - anterior cord which the result of fracture or dislocation to the anterior aspect of the spinal cord - brown square which when only the right or left side of the spinal cord is effected - Cauda equina where there is injury at or below the L2 regions and extends to the lumbar and sacral regions of the spinal cord.

Answer 63

Complete spinal cord injuries are those in which there is complete loss of innervation below the site of injury commonly resulting in paraplegia or quadriplegia. The spinal cord may or may not be severed. Quadriplegic – partial or total loss of function of all four limbs therefore the SCI needs to have occurs above T2 hence the arms and legs can no longer be innovated. Paraplegic – only the lower two limbs are effected this means that the injury needs to occur below T2. You can have paralysis of the arms and not the legs in SCI The incomplete injury is when the patient has sensory and motor functions which extends below the injury site hence some nerve pathways remain intact. The common types of incomplete injury include - central cord syndrome - brown sequard - anterior cord

Answer 64

Spinal cord injuries can be classified through 1. The mechanism of action ( mechanical, toxic, ischaemic ) 2. Type of cord injury ( Anterior cord, Central cord, Brown Sequard, Cauda, complete or incomplete ) 3. The degree of disability ( paraplegic or quadriplegic )

Answer 65

Either mechanical, toxic or ischaemic Mechanical - shearing (when different aspects of the spine go in opposing directions typically de to force / trauma) - crushing (spinal cord is crushed due to compression typically de to force / trauma) - axial loading / compression (squashing from head) - distracting / tension (hanging / stretching) - torsion (twisting) - skeletal degeneration (osteoarthritis or disk degeneration) - malignancy (tumors) Toxic : - infections (Encephalitis) - autoimmune disease (mistakenly attacks the spinal cord) - Acids / Alkalis (exposure to these substances can cause cell death within the spinal cord. Ischemic : - primary ischemia is when the cells die instantly, immediately when the car hit the tree they died causing SCI. - secondary ischemia is when the cells due hours or days post incident due to tissue hypoxia, decreased perfusion status, swelling.

Answer 66

Status Epilepticus is when a seizure has lasted longer than 5 minutes or the patient has reseized within their post ictal phase before regaining their full GCS. This is classified as a medical emergency as the brain is continually deprived of oxygen and glucose which means that the cells in the brain become ischemic as they cannot survive without oxygen. This loss of oxygen causes the body to generate energy through anaerobic metabolisms therefore increasing the levels of lactic acid within the body which disrupts electrolyte balances and therefore further metabolic challenges. As well as this there is an imbalance in ions and therefore neurotransmitters release this causes cardiac arrythmias due to the abnormal cardiac conduction and increased excitability of cells. Respiratory complications may also arise due to the effects that the seizure has on the brain stem which regulates breathing and may cause none to irregular breathing. As well as this because the patient may be unconscious there is a risk that they aspirate on their saliva or vomitus due to their inability to maintain a patent airway. Also impaired breathing impairs gas exchange which will further contribute to hypoxia. - respiratory - cardiac - hypoxia and glucose deprivation

Answer 67

Midazolam binds to the GABA receptors to change the receptor shape to increase its affinity for GABA to bind. This then open the ion channels to allow for chloride to enter the cell hyperpolarising it hence making it more negative. This means that a larger stimulus is required to depolarise the cell. This if effective in a stopping a seizure as there is abnormal electrical discharge coming from the neurons within the brain and therefore if we hyperpolarise the cell these neurons cannot be stimulated as effectively hence stopping the seizure. The dosage for midazolam is 0.1mg/kg to a max of 10mg per patient and 5mg per injection site. Keppra is another medication that can be administered by an ICP’s to stop a seizure, we use this medication after 2 doses of midazolam. Keppra stops the release of glutamate from the presynaptic neuron by blocking the protein that releases the vesicles. As glutamate is an excitatory neurotransmitter less glutamate means that there is less excitatory drive within the cells leading to decrease neuronal activity as the cell becomes more negative.

Answer 68

Seizures are defined as an inappropriate electrical discharge resulting in disordered brain activity, where there is a diagnosis and a known cause and trigger points for the patient. Epilepsy is defined as a condition where there is repetitive but largely unpredictable episode is of seizure activity where there is not cause and the seizure activity cannot be linked or diagnosed.

Answer 69

The temporal lobe of the brain controls, memory, hearing, behaviour and language comprehension. Therefore seizure activity within this aspect of the brain can present in a variety of different ways. Temporal lobe epilepsy is classified as a behavioural seizure, some patients may manifest with automaticity where they continue with whatever they are doing but with no conscious awareness. This may be driving a car and getting to your destination but cannot recollect the car ride. Other presentations may manifest with violent behaviour, or sexually inappropriate behaviour but not all patients with temporal lobe epilepsy experience altered consciousness some may experience hallucinations alterations to their perception or changes in personality.

Answer 70

Focal seizure : a focal seizure is one where the electrical activity in the brain stays isolated to one area within the brain. There are two types of focal seizures aware and impaired, aware focal seizures are those that the patient remains conscious and manifests depending on its location within the brain typically it presents a small tics and small muscle movements lasting about 30-60 seconds. Whereas impaired focal seizures are ones that the patient has an altered consciousness where the patient is unconscious or unaware of their actions and the presentation depends on its location within the brain but typically is hand flashing or face washing movements lasting 30 seconds - 2 mins. Generalised seizure : this is where the seizure may occur in either one hemisphere or both hemispheres of the brain. A common type of generalised seizure includes myoclonic epilepsy where the seizure is isolated to a muscle or limb whereas a tonic clonic seizure is marked as the tonic movements of rigidity and clonic being the rhythmic convulsions of the muscles. Individuals with tonic clonic seizures are typically unconscious or if they are conscious they are unable to control the muscle movements typically resulting in incontinence. Anther generalised seizure includes the absence seizure, this is where the patient remains conscious, but they have no concept of time and loses their awareness and freezes or stares into the distance. There are minimal other manifestations, but this only lasts for 30 seconds but people may have numerous absence seizures in 1 hour.

Answer 71

Epilepsy is common medical condition within the younger as their brains are still developing and elderly due to the higher risk of neurodegenerative and neurological disturbances and males having a higher prevalence over females due to hormonal differences. As well as this the population of people in higher socioeconomical areas have a lower rate of epilepsy when compared to those of a lower economic group, this it thought to be attributed to the higher classes access to medical treatment and interventions. - elderly and youth - higher in poorer populations bc they don’t have access to medical treatment

Answer 72

Epileptic focus is a region within the brain wither hyperexcitable neurons that produces abnormal electrical discharges, this discharge then spreads to other areas of the brain and leads to a seizure. In some individuals this group of neurons can be surgically removed when the condition becomes severe to life threatening, this will reduce the amount and risk of future seizures but doesn’t not work for all cases.

Answer 73

A TIA is a type of ischemic stroke which becomes dislodged and self resolves within 24 hours without medical intervention. The patient will experience symptoms of a stroke but these will self-resolve also hence no permanent damage will occur. Usually, a TIA is an indicator of underlying thrombotic disease and is a warning to the person that they are at high risk of stroke.

Answer 74

ACT is an assessment tool that we can use in the prehospital setting to becomes highly suspicious of a large vessel occlusion. This is to be performed after a ROSIER where it further assesses the arm weakness. Right arm weakness = chat so the patient will have a severe language deficits, which includes incomprehensible and gibberish conversation Left arm weakness = tap so when you tap the patient on the shoulder they will gaze / deviate both eyes to the opposite side in which they were tapped or failure to turn to the weak side. If the patient fails to complete either of these tasks they become ACT positive and therefore have a large vessel occlusion. Being ACT and ROSIER positive means that a patient should be transported to the RAH on priority with code stroke activation. The RAH can perform the correct medical imaging as well as thrombolysis which is the administration of tissue plasminogen activator which will break down the clot and a thrombectomy where the clot is removed.

Answer 75

ROSIER is an assessment tool that is conducted on patient that are suspected to have a CVA. This involves assessing majority of the lobes within the brain for the onset of new neurological symptoms where a stroke may be suspected. This involves; When was the patient last seen well or without the new onset of neurological symptoms? - LOC ? - Seizure activity ? - Facial weakness - Speech disturbances - Visual field defects - Asymmetrical arm weakness - Asymmetrical leg weakness - Pre-morbid independence (if they have a good quality of life and are going to survive this) - must have a BGL above 3.5 (or they are considered to by in a hyopglycaemic episode If the patient has any of these symptoms with a new onset in the previous 24 hours they receive a +1 or a -1 for seizure and LOC. the score can be graded from -2 through +5. If there is arm weakness progress onto ACT to determine large vessel occlusion.

Answer 76

The clinical manifestations of a CVA are dependant of where the occlusion within the brain, the further away from the Circle of Willis the more minute the signs and symptoms will appear as they are preventing blood flow to a smaller area of the brain causing ischemia. When compared to a large vessel occlusion this displays more widespread manifestations as the area of ischemia is much larger and therefore a larger portion of the brain is unable to function correctly. The diagnosis of a CVA is impossible in the prehospital setting as it requires medical imaging to determine but we can be extremely cautious and suspicious. Knowing this a comprehensive patient assessment is to be undertaken on any patient whom has symptoms of a stroke, or suspicion of a stroke, or altered consciousness due to neurological decline. The prehospital management for a CVA is early recognition using a ROSIER and ACT assessments. Reassurance to the patient as they will be very confused and scared as part of their brain is still functioning properly therefore they may be aware what is going on but not able to articulate tit due to the speech impairment. A prioritised set of neuronal observations and holistic observations and continual reassessment and monitoring for any alterations. Activating code stroke with notification enroute to the correct hospital / stroke unit. This will allow the receiving department either RAH for large vessel occlusions or RAH, flinders or Lial MAC for code stroke to have their team and equipment prepared for intervention.

Answer 77

A cerebrovascular accident (CVA) is a localised vascular lesion that develops suddenly within the cerebral circulation where the vessel bleed or become blocked. This results in a cerebral infarct where the neurons within the affected area become deprived of oxygen and glucose and hence are damaged. There are two types of CVA ischemic and haemorrhagic Ischaemic strokes : Ischaemic strokes are caused by a blood clot and therefore oxygen and glucose deficiency to aspects of the brain. Sudden obstruction of a cerebral artery can be due to thrombus or an embolus. An embolic stroke is from a blood clot that has formed in previous areas of the body and travel via the bloodstream to the brain causing damage - DVT Within a thrombosis the blood flow is affected due to the narrowing of the vessels due to atherosclerosis, this build up will eventually constrict vascular flow causing blood clotting formation and hence thrombotic ischaemic stroke. Can be two types : 1. Cerebral vascular accident which is Permanent without intervention 2. Trans ischaemic attack (TIA) which can Self-resolve without intervention Haemorrhagic strokes : Haemorrhagic stroke occurs when a cerebral artery ruptures typically from an aneurysm and there is a bleed within the brain tissue, in addition to the loss of blood supply the haemorrhage can greatly displace brain tissue due to the increased intracranial pressure. There are 4 subcategories of haemorrhagic strokes; 1. Subarachnoid haemorrhage o A subarachnoid haemorrhage is bleeding between the dura matter and the pia matter layers of the brain known as the subarachnoid space. 2. Subdural haemorrhage o an accumulation of blood between the arachnoid matter and the dura mater of the brain. 3. Epidural haemorrhage o An accumulation of blood between the dura matter and the skull 4. Intracerebral haemorrhage o A bleed within the brains parenchyma The major risk factors for stroke are; - hypertension - diabetes mellitus - hyperlipidaemia / hypercholesterinaemia - smoking, age - family history / genetics - alcohol consumption - heart disease and or cardiovascular abnormalities, such as AF - heritage : pacific islander, African-American, Indigenous Australians - TIA history +++ - Obesity - Excessive alcohol use - Age over 55 - Coronary artery disease - Insufficient physical inactivity and poor diet - birth control (pill) With the cardiovascular risk factors for a CVA there is a complication between individuals with atrial fibrillation and their left atrial appendage a small, pouchlike sac within the left atria. The appendage as well as the turbulent flow and stagnant blood creates a favourable environment for clot formation. Once the clot forms it can dislodge from the atrial appendage and enter the systemic circulation travelling to the brain with the potential of causing an embolic ischaemic stroke.

Answer 78

GCS - assesses the alertness and mental consciousness of a patient Given in a score of 15 with 3 being the lowest which is an unresponsive patient Best eye response (4) 1. No eye opening 2. Eye opening to pain 3. Eye opening to sound 4. Eyes open spontaneously Best verbal response (5) 1. No verbal response 2. Incomprehensible sounds 3. Inappropriate words 4. Confused 5. Orientated Best motor response (6) 1. No motor response. 2. Decelerate - drop cat long arms 3. Decorticate - catch cat arms in 4. Withdrawal from pain 5. Localizing pain 6. Obeys commands

Answer 79

The 7 different levels of consciousness consis of CCDLOSC conscious cathy dances lots of school concerts 1. Fully conscious - awake and alert 2. Confused - disorientated to time and confused speech 3. Delirium - separated from reality, may experience hallucinations and delusional thoughts 4. Lethargic - drowsy but can be aroused 5. Obtundent : more drowsy than lethargic less interested in their environment and slowed responses 6. Stupor - can only be aroused by painful stimulus and goes back to unresponsive when not stimulated 7. Coma - completely unresponsive and cannot be aroused

Answer 80

Endogenous analgesia are the opioids that the body releases in relation to pain these are endorphins, enkephalins and dynorphins. Therefore Endorphins bind to Mu, enkephalins bind with delta and dynorphins bind with kappa. Their structures allow them to have a high affinity for their primary receptors but when required they can bind to the other receptors. These are useful in pain pathways as they are primarily located within the CNS and spinal cord therefore they begin to inhibit the release of glutamate and substance P from the presynaptic neuron and inhibit the depolarisation of the postsynaptic neuron. This action occurs can occur at any of the locations of the opioid receptor and their synapse. These are useful as they initiate pain relief pathways before the use of exogenous opioids. Mu are located in the brainstem, thalamus, cortex and dorsal horn. Delta are located in the cerebral cortex and amygdala Kappa are located in the spinal cord, limbic system, dorsal horn, hypothalamus and brainstem Also in the descending pain pathway is the PAG and RVM. The PAG is the neuron that goes from the cortex to the midbrain that carries the main output or action wanted from the limbic system. The PAG then synapses with the RVM at the midbrain and continues through to the dorsal horn where it synapses at the same location that the 1st and 2nd order neurons synapsed and begins to inhibit the release of substance P from the presynaptic neuron by inhibiting the influx of calcium by binding to voltage gated calcium channels hence stopping the release of substance p. As well as this enkephalins also add to the reduction the release of substance P from the presynaptic neuron by opening potassium channels and enhancing potassium efflux from the cell as well as stopping calcium from entering. Also inhibiting the depolarisation of the post synaptic neuron by binding to voltage gated calcium channels and stopping the influx of calcium hence stopping the release of substance p therefore stopping the conduction of the pain pathway due to hyperpolarisation.

Answer 81

Ketamine : Acts on the NMDA receptors in the thalamus to stop glutamate from binding the transmission of pain signals into the cortex for processing. This means that it is inhibiting the third order neurons. Dependant on the dose of ketamine will depend on the degree of its effect in relation to the ketamine curve. It can bind to the opioid receptors but has a higher affinity to NMDA receptors. - Muscarinic and nicotinic receptors agonist of the parasympathetic nervous system – that why patients can hypersalivate - Alpha and beta agonist in the sympathetic nervous system (increase in BP and HR) 10mg / kg is the recommended dose for analgesia this means that it binds to the opioid receptors (u, delta, kappa) at the dorsal horn and inhibits the release of substance P. 50mg / kg is used for partial dissociation where the medication will partially inhibit the thalamus’s actions and therefore no signals will reach the cortex for processing. This increases a patient’s risk of an emergent reaction. As there is still some signals being process and the brain is trying to work out what is happening hence hallucinations, bad dreams, feeling strange. 100mg / kg is complete dissociation this means that the cortex is not receiving any stimuli from the thalamus and peripheries.

Answer 82

First order neurons are those that transmit pain stimuli from the site of injury into the dorsal horn. These can be either alpha/delta fibres which are myelinated fibres hence travel much faster and provide sharp instant pain or C fibres which are unmyelinated fibres which carry the slower pain signals. We can only manipulate c fibres and their pathways - You have your patient arm break pain under control but when you hit a bump, they have increased pain due to the ad fibres. - Inhibited by localised anaestetic – lignocaine Second order neurons synapse with first order neurons within the dorsal horn and receive the pain transmission via substance P neurotransmitters. By binding to the opioids receptor substance p relays the information to the second order neuron which then crosses the spinal cord and ascends up the spinothalamic tract and into the thalamus where is synapses with the third order neuron. - Dorsal horn inhibited by endogenous and exogenous opioids Third order neurons synapse with the second order neuron in the thalamus the third order neuron goes from the thalamus to the cortex to the specific region of the location of the injured site. - Inhibited by ketamine

Answer 83

Mu : pre and post synaptic (dorsal horn, brain stem, thalamus cerebral cortex) Delta : post synaptic (Cerebral cortex and amygdala (fight / flight) ) Kappa : post synaptic (limbic system, hypothalamus, brainstem, spinal cord)

Answer 84

Nociception is the pathological process of sensing a noxious stimuli that can result in harm to the tissues. It detects different pressures such as heat, temperature, and noxious stimuli. Pain is referred to as a subjective experience that is the result of nociception activation following the pain pathway and is process by the cortex. This stimuli is perceived within the brain due to a variety of influencing factors including emotional, physical and psychological experienced previously. Therefore pain can be perceived differently by all individuals but nociception stimulation is the same for everyone.

Answer 85

Hyperalgesia : is the increase in pain perception which may be caused by a range of effects within the pain pathways and descending pathways but most commonly caused by the inflammatory medicators at the site of injury making the membrane potential closer to the threshold potential. An example of this is post surgery what would normally be considered mild pain to the patient is now considered severe pain due to these imbalances. Allodynia : this is when something that should not cause pain causes, causes pain. This is due to any abnormalities within the pain pathway and processing but is commonly caused due to central sensitization which is a change to your central nervous system that increases you sensitivity to pain. An example of this is when you touch your arm it should hurt but it really does hurt. Changing the sensitivity of the neurons through changes in the peripheries, spinal cord and brain restricting the use if the injured limb in order to facilitate healing and prevent re-injury. As the wound heals the mechanisms that led to the injury hyperalgesia and allodynia should be reversed restoring the high-threshold character of the nociceptive neurons. The inability to reverse this process is considered to become neuropathic pain.

Answer 86

Productive pain is the immediate pain associated with the injury present, hence is the pain perceived at the time of injury. Non-productive pain is the ongoing pain post injury or the painful experience due to the ongoing changes to the surrounding neurons.

Answer 87

Pain is subjective due to biological, psychological and social factors. These include your biological response to pain which is determined through nociceptors, stimulus and potential spinal cord injuries, genetic factors also play a role in the subjective sensation of pain, as males typically have a higher pain threshold and hence their pain is taken more seriously when compared to women. The psychological factors include if you’ve experienced the pain before (Hyperalgesia or Allodynia) hence potentially making the sensations worse or you’re more scared or you have less pain tolerance as you know how it feels. Also social / stereotypes / cultural factors can influence out pain as males may not feel manly if they say they are in pain rather females are more ‘prone’ to pain and crying hence their pain is taken less serious. Also culturally men may need to be the father figure and not displayed their pain. Pain is also a perception due to previous experience both emotionally, physically and pathologically therefore MMA fighters may not feel a stubbed toe as i would because they are constantly being injured.

Answer 88

Paediatric pain assessment looks at the patient facial expressions / the FLACC scale assessing movement as a way of rating their pain. Each scoring either a 0,1,2 for their presentation 0. Normal presentation 1. Can be helped but 2. Bad • Face • Legs • Activity • Cry • Consolability For adults we can assess pain through the use of DOLOR • Description of pain • Onset of pain • Location of pain • Other signs and symptoms • Relievers – medication / posture • Pain score out of 10

Answer 89

Neuropathic pain refers to the pain initiated by a primary lesion or dysfunction in the sensory cortex, it can be either generalised, symmetrical or localised and commonly presents as electrical or burning like sensation. This is due to an alteration in the descending pathways where there is an imbalance in the excitatory and inhibitory neurotransmitters therefore decreasing descending pathways capacity to modulate pain. Chronic pain is pain that persists beyond the typical recovery period for that injury, this is due to the long standing inflammatory processes in which make the threshold potential closer to the membrane potential therefore increasing the sensitivity of pain. As well as this central sensitisation of the neurons in the CNS by increasing their excitability will make them more response to smaller stimuli.

Answer 90

Endogenous analgesia are the opioids that the body releases in relation to pain these are endorphins, enkephalins and dynorphins. Therefore Endorphins bind to Mu, enkephalins bind with delta and dynorphins bind with kappa. Their structures allow them to have a high affinity for their primary receptors but when required they can bind to the other receptors. These are useful in pain pathways as they are primarily located within the CNS and spinal cord therefore they begin to inhibit the release of glutamate and substance P from the presynaptic neuron and inhibit the depolarisation of the postsynaptic neuron. This action occurs can occur at any of the locations of the opioid receptor and their synapse. These are useful as they initiate pain relief pathways before the use of exogenous opioids. Mu are located in the brainstem, thalamus, cortex and dorsal horn. Delta are located in the cerebral cortex and amygdala Kappa are located in the spinal cord, limbic system, dorsal horn, hypothalamus and brainstem Also in the descending pain pathway is the PAG and RVM. The PAG is the neuron that goes from the cortex to the midbrain that carries the main output or action wanted from the limbic system. The PAG then synapses with the RVM at the midbrain and continues through to the dorsal horn where it synapses at the same location that the 1st and 2nd order neurons synapsed and begins to inhibit the release of substance P from the presynaptic neuron by activating the g protein in which reduces the amount of cyclin AMP to reduce the functions of the voltage gated calcium channels hence stopping the release of substance p. As well as this enkephalins also add to the reduction the release of substance P from the post synaptic neuron by opening potassium channels via the same process of activating the g protein in which reduces the amount of cyclin AMP to reduce the functions of the voltage gated potassium channels and enhancing potassium efflux from the cell. This causes hyperpolarisation of the cell and therefore the post synaptic neuron will need a larger stimuli than normal to generate another action potential to permit the stimulus.

Answer 91

The endogenous agonists (endorphins, enkephalins and dynorphins) from binding to the post synaptic neuron by blocking the endogenous receptors (Mu, Delta and Kappa). In the presence of the endogenous opioids, within the synapse they inhibit the influx of calcium into the presynaptic neuron (1st order neuron) by stimulating the G protein in which reduced the amount of cyclin AMP which reduces the function of the voltage gated calcium channels from opening therefore the NT’s aren’t able to leave the presynaptic neuron and in the same process by stimulating the G protein in which reduced the amount of cyclin AMP which reduces the function of the voltage gated potassium channels the post synaptic neuron becomes hyperpolarised and therefore needs a larger stimuli to depolarise hence stopping the noxious pathway.

Answer 92

Aδ and C fibres are the two types of nociceptors neurons, each associated with different types of pain that travel from the site of injury to the dorsal horn as pieces of the ascending pain pathway. - Aδ fibers : are myelinated axons hence are fast transporting impulses they interpret sharp, localised pain. - C fibers : are unmyelinated axons hence have a slow transition that interpret dull sensations and aching pain, opioid medications are able to inhibit these pathways thorough the descending pathways. We can give opioid medication that reduce ones pain hence manipulating the c fibres but if the ambulance hits a bump and the patient jerks this is a type of Aδ fibre transmission therefore the patient is still going to feel that pain as it is a fast, sharp pain.

Answer 93

to inhibit pain pathways, it can either be through the presynaptic neuron, this would be through the endogenous or exogenous opioids binding to the opioid receptor either mu, delta or kappa. The endogenous opioids will bind to their receptor molecules on the presynaptic cleft and therefore activate a g protein, this will then reduce cyclin AMP which will reduce the activity of the voltage gated calcium channels to reduce the influx of calcium into the cell. This will then reduce the amount of substance P and glutamate from being released into the synapse and therefore reduce the transmission of noxious stimuli. On the post synaptic membrane the opioid bind to the opioid receptors and again activate the g protein in which reduced the amount of cyclin AMP within the cell and in turn enhances the activity of the voltage gated potassium channels to allow for the efflux of potassium out of the cell. This leads to hyperpolarisation of the cell therefore it will need a larger stimuli than normal to depolarise therefore inhibiting the noxious stimuli transmission pathway.

Answer 94

Central Nervous System : is characterised by the brain and spinal cord, this involves the processing of sensory input and generates motor output. Peripheral Nervous System : this involves all of the tissues that are outside the CNS. This can be further broken down into the somatic nervous system and the autonomic nervous system SNS control voluntary movements and conscious control of muscles and relays sensory information to the spinal cord. ANS controls involuntary functions, HR, digestion and respiratory rate. This can be broken down into sympathetic and parasympathetic. Where parasympathetic counterbalances the effects of the sympathetic for the body to recover and repair. - sympathetic : fight or flight heightens all unconscious aspects (increase HR, redistribution of BP) - parasympathetic : vagus nerve initiates rest and digest (decrease HR, increase salivation and digest)

Answer 95

Dendrites : receive signals from neurotransmitters Cell body : where the nucleus and organelles (mitochondria) are located and is responsible for the neuron’s health. Axon hillock : this is where the cell body turns into the axon, this is also the location for the voltage gates sodium channels to allow for the depolarisation of the neuron. Axon : this is the connection between the dendrites and the axon terminal. This is responsible for the propagation of the message. Myelin sheaths : made of Schwann cells and Oligodendrocytes, these insulated covering surround parts of the axon to increase the speed of transmission of the nerve impulse. Node of Ranvier : the segments of the axon that are in between the myelin sheaths. Axon terminal : this is where the neurotransmitters are release into the synaptic cleft in response to the influx of calcium

Answer 96

There are 4 different types of neurons : 1. Anaxonic neurons : these are neurons where the cell body and dendrites are the same thing, located in the brain and special sense organs. 2. Unipolar neurons : the cell body is attached to the axon, these transmit sensory information hence located within the peripheral nervous system 3. Bipolar neurons : these neurons are those that have the cell body embedded within the axon, these are located within sense organs and relay senses of sight, smell and hearing. 4. Multipolar neurons : these are the most common where the cell body in embedded within the dendrites, these consist of all motor neurons.

Answer 97

Schwann cells are the myelinated sheaths surrounding the axons, they allow actions potential to travel through the axon at a much faster rate as well as protecting the axon from damage by interstitial fluid. Satellite cells are located around the cell bodies in the peripheral nervous systems ganglia and regulate the chemical environment surrounding the neuron, and balance neurotransmitters and ionic movements in and out of the cell.

Answer 98

There are different membrane potentials in all modes of conduction and transmission. This allows for the propergation and movement of things. Resting membrane potential : -70 This is the normal potential of the membrane in its resting state. - the movement of a positive ion comes into the cell (sodium, calcium) Threshold potential : -60 this is point at which the voltage gated ion channels open and allow the semi rapid influx of positive ions. This is when the action potential in generated from. - the rapid influx of positive ions via voltage gated channels cause this to rise to +10 then the voltage gated channels inactivate as they have reached potential but the voltage gates potassium channels open to make the cell more negative and return it back to its normal resting membrane. They shut off at 0 and -60 but there is some overflow Action Potential : the depolarisation of the neuron which allows the transmission of a signal from the dendrites to the axon terminal. - the action potential depolarises down both sides of the neuron and meet in the middle of the axon terminal Synapse activity : this is where the neurotransmitters are released into the synapse. for this to occur the depolarisation triggers the entering of calcium into the axon terminal and hence exocytosis can occur with the neurotransmitters. They go into the synapse and bind with the receptors on the post synaptic membrane.

Answer 99

There are different membrane potentials in all modes of conduction and transmission. This allows for the propergation and movement of things. Resting membrane potential : -70 This is the normal potential of the membrane in its resting state. - the movement of a positive ion comes into the cell (sodium, calcium) Threshold potential : -60 this is point at which the voltage gated ion channels open and allow the semi rapid influx of positive ions. This is when the action potential in generated from. - the rapid influx of positive ions via voltage gated channels cause this to rise to +10 then the voltage gated channels inactivate as they have reached potential but the voltage gates potassium channels open to make the cell more negative and return it back to its normal resting membrane. They shut off at 0 and -60 but there is some overflow Action Potential : the depolarisation of the neuron which allows the transmission of a signal from the dendrites to the axon terminal. - the action potential depolarises down both sides of the neuron and meet in the middle of the axon terminal Synapse activity : this is where the neurotransmitters are released into the synapse. for this to occur the depolarisation triggers the entering of calcium into the axon terminal and hence exocytosis can occur with the neurotransmitters. They go into the synapse and bind with the receptors on the post synaptic membrane.

Answer 100

Resting membrane potential is around -70 and is created through the sodium potassium pump, when the resting membrane potential is above -70 (-65) the sodium potassium pump allow the small influx of potassium into the cell and as this is a negative ion is reduces the membrane potential - hyperpolarsing the cell and reverse for when the cell is at -75 it allow a small influx of sodium to increase it back to -70 - hypopolarising the cell. As the extracellular fluid is more positive as it contains a larger amount of sodium and chloride ions the intracellular fluid is more negatively charged as it contains more potassium ions. As the cell wall is semi permeable there can be slow leakage of ions across this membrane but it is typically controlled by the sodium potassium pump.

Answer 101

Grey matter is the H like structure in the middle of the spinal cord where the organelles are located this is also the site of the dorsal horn where the first and second order neurons synapse. The white matter is the surrounding material of the grey mater and is the location of the ascending (sensory) and descending (motor) pathways. The spinal cord is separated into 4 different areas 1. Cervical C1-C8 - innervates head till front of arms 2. Thoracic T1-T12 - innervates back of arms till pelvis 3. Lumbar L1-L5 - innervates front of legs 4. Sacral S1-S5 - innervates back of legs and baldder The phrenic nerve leaves the spinal cord at C3-C5 At each exit point on the spinal cord, where the nerve leaves there is a dorsal or ventral ganglion that synapses with another neuron. The spinal cord is made three layers the dura matter, the outside layer, the arachnoid matter, the middle layer and the pia matter the layer closes to the bone. These layers help protect and insulate the spinal cord.

Answer 102

The main regions of the brain include 1. Frontal lobe : speaking, motor control, emotion, problem solving and judgement 2. Parietal lobe : proprioception, knowing left from right, sensations, reading. 3. Temporal lobe : hearing, language comprehension, behaviour, memory 4. Occipital lobe : vision and colour perception 5. Brainstem : involuntary actions, breathing, HR, swallowing, digestion 6. Cerebellum : balance, coordination of voluntary movements, fine muscle control

Answer 103

The spinal cord is separated into 4 different areas 1. Cervical C1-C8 - innervates head till front of arms and the forearm 2. Thoracic T1-T12 - innervates back of arms till pelvis 3. Lumbar L1-L5 - innervates front of legs 4. Sacral S1-S5 - innervates back of legs and baldder The phrenic nerve leaves the spinal cord at C3-C5

Answer 104

1. Cerebrum 2. Diencephalon : diencephalon, thalamus and hypothalamus 3. Cerebellum 4. Brain stem : midbrain, pons, medulla Cerebrum : divided into left and right hemispheres, controls conscious through, memory storage, sensory processing and skeletal muscle control. - Fissures are deep groves that subdivide each cerebral hemisphere - Gyri are folds in the cerebral hemispheres that increase its surface area - Sulci are shallow groves in the cerebral hemispheres that separate adjacent gyri Diacephalon : is the structural and functional link between the correct and the brain stem it contains the thalamus (relaying sensory information) and hypothalamus (control of emotions autonomic functions and hormone production) Brainstem : comprised of the midbrain, pons and medulla. - Midbrain processes the visual and auditory, maintains consciousness and somatic motor responses - Pons : the bridge between the medulla and the midbrain - Medulla : relays sensory information to teh thalamus, regulates cardiovascular, respiratory and digestive systems Cerebellum controls balance and conscious movements, adjusts output from the somatic motor centres in the brain and spinal cord

Answer 105

The spinal cord can function with no input from the brain due to autonomic innervation. This includes the sympathetic and parasympathetic nervous systems. Originating from the thoracic and lumbar regions the sympathetic nervous system controls the fight or flight response hence innervates responses to stress by increasing HR and vasodilation. Originating in the sacral region the parasympathetic nervous system opposes the sympathetic nervous system which promotes resting and digest, reducing heart rate and vasoconstriction once the sympathetic has done its job. Blood pressure regulation through the baroreceptors therefore not needing the brains input but adapting through either the sympathetic or parasympathetic nervous systems innervations. Reflex actions / arch’s : this is a neural pathway that enable the immediate response to noxious stimuli. The stimuli travels via a sensory neuron to the spinal cord where it synapses with an interneuron and then a motor neuron to have the effect on the muscle, gland or adipose tissue. EG, finger on hot plate — sensory neuron — spinal cord — interneuron — motor neuron — exit spinal cord — contracts biceps to pull finger away from heat.

Answer 106

Dura matter - outer most layer, toughest layer, protection. Arachnoid matter - middle layer, web like structure filled with CSF to provide the brain with cushion Pia matter - inner most layer, thin membrane with blood vessels, supplies blood and oxygen to spinal cord.

Answer 107

Every segment of the spinal cord is connected to a pair of spinal nerves, the spinal nerve is formulated when both the ventral and dorsal roots connect together. these nerves are covered with a 3 layers of connective tissue and within these layers there are arteries, veins and fascicles in which encompass the neurons.

Answer 108

The brain is protected from the external environment by the skull, hair and skin. Internally from the skull there are the meninges, the dura matter which is a thick protective layer attached to the skull, then there is the arachnoid matter which consists of a weblike structure that contains the CSF and supports its circulation and finally the Pia matter which is the closest layer to the cortex. This layer contains all the blood vessels and provides the brain with oxygenation it requires. CSF is produced by the choroid plexus within the ventricles in the brain, it transports nutrients and chemical to and from the brain, supports the metabolic processes and maintains homeostasis within the brain. It is continually being synthesised and absorption to allow for a stable volume and pressure within the CNS. Within the CSF there are issues with hydrocephalus where the CSF is imbalanced resulting in its accumulation within the brain. There are 4 different types of hydrocephalus 1. Communicating hydrocephalus : this is when the CSF is unable to be reabsorpted hence builds up 2. Obstructive hydrocephalus : where there is a blockage in the conduction pathways hence it becomes stagnant 3. Normal pressure hydrocephalus : there is an increase in CSF causing ventricular enlargement without an increase in ICP 4. hydrocephalus ex vanco : this is when ventricles enlargement due to brain atrophy and therefore needs more CSF - common in alzheimers.

Answer 109

1. Stimulus 2. Depolarisation of a receptor : there is a change in membrane potential of a receptor cell 3. Action potential generation : the membrane potential reaches threshold and an action potential is depolarised. The longer the depolarisation the higher the frequency of action potentials 4. Propagation over labelled line : axons carrying information about a stimuli. The CNS interprets the stimulus according to which label is activated. 5. CNS processing : the brain processes the information 6. Motor pathways : a. Involuntary : processing centres in the spinal cord or brainstem may direct an immediate reflex response even before sensations reach the cerebral cortex b. Voluntary : not immediate, can moderate, enhance or supplement the relatively simple involutory reflexive response – enables a movement that is voluntary

Answer 110

Receptors can be classified according to the nature of the stimuli Nociceptors : pain receptors that do not adapt quickly. These free nerve endings have large receptive fields. Two types of axons - Alpha Delta fibres – propagate actions potentials faster and respond to less intense stimuli. fast pain (pin prick) trigger somatic reflexes which are generally relayed to the primary somatosensory cortex and so receive conscious attention. Fast acting as they neurons are myelinated - C fibres – slower unmyelinated neurons are slow pain. Caused by generalised activation of the reticular formation thalamus. The person becomes aware of the pain but only has a general idea of the area affected (abdominal pain) Thermoreceptors : temperature receptors, the nerve endings are located in the dermis of the skin, skeletal muscles, liver and hypothalamus. There are cold and warm receptors but have no structural differences but there are 3-4 times more cold receptors than warm Mechanoreceptors : stimuli that distorts their plasma membranes, chemically gated ion channels whose gates open and close in response to stretching, compression, twisting or other distortions of the membrane. - Proprioceptors – monitor the position of joints and muscles. Muscle spindle - Baroreceptors – detect pressure changes in the walls of the blood vessels and in portions of the digestive, respiratory and urinary tracts - Tactile receptors – sensation of touch (shape and texture), pressure (frequency of mechanical distortion) and vibration. o Fine touch pressure receptors – provide detailed information about a stimuli o Crude touch and pressure receptors – poor localisation and give little information Chemoreceptors : respond to water-soluble and lipid-soluble substances that are dissolved in body fluids (interstitial fluids, blood and CSF)

Answer 111

Spinothalamic pathway : conscious sensation of poorly localised touch, pressure, pain and temperature. Axons of first order neurons enter the spinal cord and synapse on second order neurons within the posterior gray horns. The axons of these interneurons cross to the opposite side of the spinal cord before ascending to the thalamus. Third order neurons synapse in the primary somatosensory cortex. 1. Anterior spinothalamic pathway – carry crude touch and pressure sensation 2. Lateral spinothalamic pathway – pain and temperature sensations Posterior column pathway : carries sensation of highly localised touch, pressure, vibration and proprioception. This pathway begins at a peripheral receptor and ends at the primary somatosensory cortex of the cerebral hemisphere. Crosses the spinal cord at the medulla oblongata. Spinocerebellar pathway : receives proprioception information about the position of skeletal muscles, tendons and joints along the spinocerebellar pathway. - The posterior spinocerebellar tract contains axons that do not cross over the opposite side of the spinal cord. These axons reach the cerebellum cortex by inferior cerebellar peduncle of that side. - The anterior spinocerebellar tracts are dominated by axons that have crossed over to the opposite side of the spinal cord

Answer 112

Spinothalamic pathway : conscious sensation of poorly localised touch, pressure, pain and temperature. Axons of first order neurons enter the spinal cord and synapse on second order neurons within the posterior gray horns. The axons of these interneurons cross to the opposite side of the spinal cord before ascending to the thalamus. Third order neurons synapse in the primary somatosensory cortex. 1. Anterior spinothalamic pathway – carry crude touch and pressure sensation 2. Lateral spinothalamic pathway – pain and temperature sensations Posterior column pathway : carries sensation of highly localised touch, pressure, vibration and proprioception. This pathway begins at a peripheral receptor and ends at the primary somatosensory cortex of the cerebral hemisphere. Crosses the spinal cord at the medulla oblongata. Spinocerebellar pathway : receives proprioception information about the position of skeletal muscles, tendons and joints along the spinocerebellar pathway. - The posterior spinocerebellar tract contains axons that do not cross over the opposite side of the spinal cord. These axons reach the cerebellum cortex by inferior cerebellar peduncle of that side. - The anterior spinocerebellar tracts are dominated by axons that have crossed over to the opposite side of the spinal cord

Answer 113

The somatic motor pathways are an aspect of the CNS that controls skeletal muscle movements. Components : It is made of upper and lower motor neurons the corticospinal tract, basal ganglia and cerebellum. The movement begins at the cortex and is relayed down the brainstem and corticospinal tract via an upper motor neuron until it synapses at the anterior horn with a lower motor. This LMN then goes to the target tissue and undergoes the effect. Through this process ACh is the main NT that is released at each of the synapses. The functions include : - voluntary movements - posture and balance - fine motor skills - reflex actions

Answer 114

Hypertension - this is because MAP trying to overcome ICP to maintain CPP Bradycardia - due to the patients increased blood pressure the barorecepros detect the increased heart rate and compensate by decreasing the heart rate Irregular respirations / channels stokes breathing - this is due to the compress of increased ICP on the respiratory centre in the medulla

Answer 115

Comprised of the - Amygdala : involved in processing emotions, especially fear and pleasure essential for the fight or flight response. - hippocampus : memory formation and learning turning short term memories into long term lessons - hypothalamus : regulates autonimic functions, hunger, thirst, sleep and temperature. Controls the release of hormones - thalamus : a relay station for sensory information The limbic system is essential in pain perception as it integrates emotions and past experiences both physical and psychological to shape the perception of pain.

Answer 116

The autonomic nervous system is divided into the sympathetic nervous system and the parasympathetic nervous system. Sympathetic is for fight or flight hence increases HR, vasodilation. It originates at T1-L2. It has short preganglion fibres and long post ganglion fibres and its main NT is ACh. Parasympathetic is for rest and digest hence it decreases heart rate and increases digestion. It originates at the cranial and sacral nerves. It has long preganglion fibres and short post ganglion fibres and its main NT is ACh. Processes : - signal transmission - innervation of HR one increases while other decreases - reflex arch’s Functions : - cardiac muscle control (increase in times of stress, decrease in times of relaxation) - smooth muscle contractions - - glandular secretion - sweat when too hot - homeostasis - regulation of blood pressure, HR, digestions and RR

Answer 117

NT release : 1. The depolarisation of the cell reaches the axon terminal, 2. This stimulates the opening of voltage gated calcium channels hence an influx of calcium enter the axon terminal 3. Exocytosis begins, the NT is contained within vesicles inside the presynaptic neuron and this binds to the cell membrane and releases the NT into the synapse 4. NT’s bind to their receptors on the post synaptic membrane. 5. If enough stimuli this then generates an action potential within the post synaptic neuron 6. The NT’s that are still left in the synapse are reuptaken by proteins or broken down by enzymes. The main NT’s in the ANS are - ACh - Norepinephrine - Epinephrine

Answer 118

Sympathetic Nervous system : main NT’s ACh, Norepinephrine, epinephrine Adrenergic - alpha adrenergic receptors ( 1 and 2 ) - beta adrenergic receptors ( 1, 2, 3 ) Parasympathetic Nervous System : ACh Cholinergic 1. Muscarinic : M1, M2, M3, M4, M5 2. Nicotine

Answer 119

the ANS maintains homeostasis at the cellular level through a variety of neurotransmitters (mainly norepinephrine and acetylcholine) that interact with specific receptors on target cells. These interactions trigger intracellular signaling cascades that lead to physiological changes, allowing the body to adapt in times of unconsciousness Cardiovascular : Sympathetic increase HR in stressful periods Parasympathetic decrease HR in response to relaxation blood pressure through the activation of the baroreceptors both mechanisms without innervation form the brain. Baroreceptors detect increase in blood pressure hence decrease heart rate to compensate. Baroreceptors detect decrease blood pressure hence increase heart rate to compensate. Respiratory : Sympathetic innervation controls bronchodilation therefore innervation breathing Parasympathetic inducing bronchoconstriction Digestive : Sympathetic causes the glands to increase sweating Parasympathetic vasodilation at rest hence conserving heat Fluid and electrolyte balance : Sympathetic reduces globular filtration rate and decreased urine output in response to stress Parasympathetic indirectly supports kidney functions hence promoted urine production in states of rest.

Answer 120

the ANS maintains homeostasis at the cellular level through a variety of neurotransmitters (mainly norepinephrine and acetylcholine) that interact with specific receptors on target cells. These interactions trigger intracellular signaling cascades that lead to physiological changes, allowing the body to adapt in times of unconsciousness Cardiovascular : Sympathetic increase HR in stressful periods Parasympathetic decrease HR in response to relaxation blood pressure through the activation of the baroreceptors both mechanisms without innervation form the brain. Baroreceptors detect increase in blood pressure hence decrease heart rate to compensate. Baroreceptors detect decrease blood pressure hence increase heart rate to compensate. Respiratory : Sympathetic innervation controls bronchodilation therefore innervation breathing Parasympathetic inducing bronchoconstriction Digestive : Sympathetic causes the glands to increase sweating Parasympathetic vasodilation at rest hence conserving heat Fluid and electrolyte balance : Sympathetic reduces globular filtration rate and decreased urine output in response to stress Parasympathetic indirectly supports kidney functions hence promoted urine production in states of rest.

Answer 121

Baroreceptors : Baroreceptors are located on the aortic arch and carotid sinus. They are involved in the homeostasis of blood pressure. They detect the stretch of the vessel walls due to the increase or decrease of blood pressure and signal the CNS to initiate the opposing effect within the heart. Increased blood pressure means decreased heart rate and vasodilation reducing sympathetic innervation, decreased blood pressure means increased heart rate and vasoconstriction reducing parasympathetic innervation. This works in a feedback loop therefore it is always detecting the changes and when they breach outside the parameters they initiate these changes. Chemoreceptors detect the alterations in oxygen to carbon dioxide ratio and pH levels. Respiratory : located on the carotid bodies and aortic bodies and detect and initiates actions in response to low oxygen or high carbon dioxide levels. When these levels are too high the chemoreceptors stimulate the CNS to increase respiratory rate and increase depth of breathing to increase the gas exchange rate at the alveolar level. Increased resp rate means there is more oxygen available to facilitate gas exchange. Metabolic : chemoreceptors located in the medulla monitor the levels of carbon dioxide and pH levels. If these levels breach their range the CNS initiates increased ventilations helping to remove the carbon dioxide and restore the pH to normal levels. pH : 7.35-7.45 O2 : 95 - 100 % CO2 : 35 - 45 mmHg

Answer 122

Due to allodynia - lowering the pain threshold and hyperalgesia - increased pain sensitivity Chronic Pain Conditions : In chronic pain conditions, sustained changes in the threshold can lead to persistent pain even after the original injury has healed. This is due to alterations in nociceptive pathways and central nervous system processing, resulting in a state of ongoing pain perception. Involvement of Neurotransmitters: in some circumstances the increased in neurotransmitter release of substance P and glutamate can lower the threshold potential and contribute to chronic pain.

Answer 123

Due to allodynia - lowering the pain threshold and hyperalgesia - increased pain sensitivity Chronic Pain Conditions : In chronic pain conditions, sustained changes in the threshold can lead to persistent pain even after the original injury has healed. This is due to alterations in nociceptive pathways and central nervous system processing, resulting in a state of ongoing pain perception. Involvement of Neurotransmitters: in some circumstances the increased in neurotransmitter release of substance P and glutamate can lower the threshold potential and contribute to chronic pain.

Answer 124

Serotonin and noradrenaline are both excitatory neurotransmitters and are released by the descending pathways to regulate and modulate pain. The RVM synapses in the dorsal horn and releases serotonin and noradrenaline into the synapse. They then have this effect … therefore by introducing SNRI’s these medication stop the reuptake of serotonin and noradrenaline therefore leaving more of these neurotransmitters within the synapse to emphasise their effects more regularly.

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